Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
A cell surface receptor for INSULIN. It comprises a tetramer of two alpha and two beta subunits which are derived from cleavage of a single precursor protein. The receptor contains an intrinsic TYROSINE KINASE domain that is located within the beta subunit. Activation of the receptor by INSULIN results in numerous metabolic changes including increased uptake of GLUCOSE into the liver, muscle, and ADIPOSE TISSUE.
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.
Glucose in blood.
A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).
A test to determine the ability of an individual to maintain HOMEOSTASIS of BLOOD GLUCOSE. It includes measuring blood glucose levels in a fasting state, and at prescribed intervals before and after oral glucose intake (75 or 100 g) or intravenous infusion (0.5 g/kg).
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.
A structurally-related group of signaling proteins that are phosphorylated by the INSULIN RECEPTOR PROTEIN-TYROSINE KINASE. The proteins share in common an N-terminal PHOSPHOLIPID-binding domain, a phosphotyrosine-binding domain that interacts with the phosphorylated INSULIN RECEPTOR, and a C-terminal TYROSINE-rich domain. Upon tyrosine phosphorylation insulin receptor substrate proteins interact with specific SH2 DOMAIN-containing proteins that are involved in insulin receptor signaling.
Maintenance of a constant blood glucose level by perfusion or infusion with glucose or insulin. It is used for the study of metabolic rates (e.g., in glucose, lipid, amino acid metabolism) at constant glucose concentration.
Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.
A syndrome with excessively high INSULIN levels in the BLOOD. It may cause HYPOGLYCEMIA. Etiology of hyperinsulinism varies, including hypersecretion of a beta cell tumor (INSULINOMA); autoantibodies against insulin (INSULIN ANTIBODIES); defective insulin receptor (INSULIN RESISTANCE); or overuse of exogenous insulin or HYPOGLYCEMIC AGENTS.
Specialized connective tissue composed of fat cells (ADIPOCYTES). It is the site of stored FATS, usually in the form of TRIGLYCERIDES. In mammals, there are two types of adipose tissue, the WHITE FAT and the BROWN FAT. Their relative distributions vary in different species with most adipose tissue being white.
Substances which lower blood glucose levels.
The ability of microorganisms, especially bacteria, to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
The ability of bacteria to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.
A 30-kDa COMPLEMENT C1Q-related protein, the most abundant gene product secreted by FAT CELLS of the white ADIPOSE TISSUE. Adiponectin modulates several physiological processes, such as metabolism of GLUCOSE and FATTY ACIDS, and immune responses. Decreased plasma adiponectin levels are associated with INSULIN RESISTANCE; TYPE 2 DIABETES MELLITUS; OBESITY; and ATHEROSCLEROSIS.
A cluster of metabolic risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components of metabolic syndrome X include excess ABDOMINAL FAT; atherogenic DYSLIPIDEMIA; HYPERTENSION; HYPERGLYCEMIA; INSULIN RESISTANCE; a proinflammatory state; and a prothrombotic (THROMBOSIS) state. (from AHA/NHLBI/ADA Conference Proceedings, Circulation 2004; 109:551-556)
Abstaining from all food.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
FATTY ACIDS found in the plasma that are complexed with SERUM ALBUMIN for transport. These fatty acids are not in glycerol ester form.
Cells in the body that store FATS, usually in the form of TRIGLYCERIDES. WHITE ADIPOCYTES are the predominant type and found mostly in the abdominal cavity and subcutaneous tissue. BROWN ADIPOCYTES are thermogenic cells that can be found in newborns of some species and hibernating mammals.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
A pathological state in which BLOOD GLUCOSE level is less than approximately 140 mg/100 ml of PLASMA at fasting, and above approximately 200 mg/100 ml plasma at 30-, 60-, or 90-minute during a GLUCOSE TOLERANCE TEST. This condition is seen frequently in DIABETES MELLITUS, but also occurs with other diseases and MALNUTRITION.
Lipid infiltration of the hepatic parenchymal cells resulting in a yellow-colored liver. The abnormal lipid accumulation is usually in the form of TRIGLYCERIDES, either as a single large droplet or multiple small droplets. Fatty liver is caused by an imbalance in the metabolism of FATTY ACIDS.
Abnormally high BLOOD GLUCOSE level.
A glucose transport protein found in mature MUSCLE CELLS and ADIPOCYTES. It promotes transport of glucose from the BLOOD into target TISSUES. The inactive form of the protein is localized in CYTOPLASMIC VESICLES. In response to INSULIN, it is translocated to the PLASMA MEMBRANE where it facilitates glucose uptake.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.
A 16-kDa peptide hormone secreted from WHITE ADIPOCYTES. Leptin serves as a feedback signal from fat cells to the CENTRAL NERVOUS SYSTEM in regulation of food intake, energy balance, and fat storage.
The processes whereby the internal environment of an organism tends to remain balanced and stable.
An indicator of body density as determined by the relationship of BODY WEIGHT to BODY HEIGHT. BMI=weight (kg)/height squared (m2). BMI correlates with body fat (ADIPOSE TISSUE). Their relationship varies with age and gender. For adults, BMI falls into these categories: below 18.5 (underweight); 18.5-24.9 (normal); 25.0-29.9 (overweight); 30.0 and above (obese). (National Center for Health Statistics, Centers for Disease Control and Prevention)
Irregular microscopic structures consisting of cords of endocrine cells that are scattered throughout the PANCREAS among the exocrine acini. Each islet is surrounded by connective tissue fibers and penetrated by a network of capillaries. There are four major cell types. The most abundant beta cells (50-80%) secrete INSULIN. Alpha cells (5-20%) secrete GLUCAGON. PP cells (10-35%) secrete PANCREATIC POLYPEPTIDE. Delta cells (~5%) secrete SOMATOSTATIN.
Consumption of excessive DIETARY FATS.
Insulin formulations that contain substances that retard absorption thus extending the time period of action.
A type of pancreatic cell representing about 50-80% of the islet cells. Beta cells secrete INSULIN.
Simultaneous resistance to several structurally and functionally distinct drugs.
Antibodies specific to INSULIN.
The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
The capacity of an organism to defend itself against pathological processes or the agents of those processes. This most often involves innate immunity whereby the organism responds to pathogens in a generic way. The term disease resistance is used most frequently when referring to plants.
A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)
Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.
Compounds which inhibit or antagonize the biosynthesis or action of insulin.
The amount of fat or lipid deposit at a site or an organ in the body, an indicator of body fat status.
Mutant mice exhibiting a marked obesity coupled with overeating, hyperglycemia, hyperinsulinemia, marked insulin resistance, and infertility when in a homozygous state. They may be inbred or hybrid.
The middle segment of proinsulin that is between the N-terminal B-chain and the C-terminal A-chain. It is a pancreatic peptide of about 31 residues, depending on the species. Upon proteolytic cleavage of proinsulin, equimolar INSULIN and C-peptide are released. C-peptide immunoassay has been used to assess pancreatic beta cell function in diabetic patients with circulating insulin antibodies or exogenous insulin. Half-life of C-peptide is 30 min, almost 8 times that of insulin.
THIAZOLES with two keto oxygens. Members are insulin-sensitizing agents which overcome INSULIN RESISTANCE by activation of the peroxisome proliferator activated receptor gamma (PPAR-gamma).
A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.
A complex disorder characterized by infertility, HIRSUTISM; OBESITY; and various menstrual disturbances such as OLIGOMENORRHEA; AMENORRHEA; ANOVULATION. Polycystic ovary syndrome is usually associated with bilateral enlarged ovaries studded with atretic follicles, not with cysts. The term, polycystic ovary, is misleading.
A 12-kDa cysteine-rich polypeptide hormone secreted by FAT CELLS in the ADIPOSE TISSUE. It is the founding member of the resistin-like molecule (RELM) hormone family. Resistin suppresses the ability of INSULIN to stimulate cellular GLUCOSE uptake.
The ability of viruses to resist or to become tolerant to chemotherapeutic agents or antiviral agents. This resistance is acquired through gene mutation.
Fatty tissue inside the ABDOMINAL CAVITY, including visceral fat and retroperitoneal fat. It is the most metabolically active fat in the body and easily accessible for LIPOLYSIS. Increased visceral fat is associated with metabolic complications of OBESITY.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
The ability of bacteria to resist or to become tolerant to several structurally and functionally distinct drugs simultaneously. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
Two populations of Zucker rats have been cited in research--the "fatty" or obese and the lean. The "fatty" rat (Rattus norvegicus) appeared as a spontaneous mutant. The obese condition appears to be due to a single recessive gene.
Polypeptides produced by the ADIPOCYTES. They include LEPTIN; ADIPONECTIN; RESISTIN; and many cytokines of the immune system, such as TUMOR NECROSIS FACTOR-ALPHA; INTERLEUKIN-6; and COMPLEMENT FACTOR D (also known as ADIPSIN). They have potent autocrine, paracrine, and endocrine functions.
The relative amounts of various components in the body, such as percentage of body fat.
A continuous cell line that is a substrain of SWISS 3T3 CELLS developed though clonal isolation. The mouse fibroblast cells undergo an adipose-like conversion as they move to a confluent and contact-inhibited state.
A protein-serine-threonine kinase that is activated by PHOSPHORYLATION in response to GROWTH FACTORS or INSULIN. It plays a major role in cell metabolism, growth, and survival as a core component of SIGNAL TRANSDUCTION. Three isoforms have been described in mammalian cells.
2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.
Substances that reduce the growth or reproduction of BACTERIA.
Insulin that has been modified so that the B-chain contains a LYSINE at position 28 instead of a PROLINE and a PROLINE at position 29 instead of a LYSINE. It is used to manage BLOOD GLUCOSE levels in patients with TYPE 2 DIABETES.
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
A pancreatic polypeptide of about 110 amino acids, depending on the species, that is the precursor of insulin. Proinsulin, produced by the PANCREATIC BETA CELLS, is comprised sequentially of the N-terminal B-chain, the proteolytically removable connecting C-peptide, and the C-terminal A-chain. It also contains three disulfide bonds, two between A-chain and B-chain. After cleavage at two locations, insulin and C-peptide are the secreted products. Intact proinsulin with low bioactivity also is secreted in small amounts.
A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289)
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
Elements of limited time intervals, contributing to particular results or situations.
A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511)
The chemical reactions involved in the production and utilization of various forms of energy in cells.
Any tests that demonstrate the relative efficacy of different chemotherapeutic agents against specific microorganisms (i.e., bacteria, fungi, viruses).
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Portable or implantable devices for infusion of insulin. Includes open-loop systems which may be patient-operated or controlled by a pre-set program and are designed for constant delivery of small quantities of insulin, increased during food ingestion, and closed-loop systems which deliver quantities of insulin automatically based on an electronic glucose sensor.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Diabetes mellitus induced experimentally by administration of various diabetogenic agents or by PANCREATECTOMY.
Regular insulin preparations that contain the SUS SCROFA insulin peptide sequence.
A monosaccharide in sweet fruits and honey that is soluble in water, alcohol, or ether. It is used as a preservative and an intravenous infusion in parenteral feeding.
Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Retinol binding proteins that circulate in the PLASMA. They are members of the lipocalin family of proteins and play a role in the transport of RETINOL from the LIVER to the peripheral tissues. The proteins are usually found in association with TRANSTHYRETIN.
A large group of membrane transport proteins that shuttle MONOSACCHARIDES across CELL MEMBRANES.
The metabolic process of breaking down LIPIDS to release FREE FATTY ACIDS, the major oxidative fuel for the body. Lipolysis may involve dietary lipids in the DIGESTIVE TRACT, circulating lipids in the BLOOD, and stored lipids in the ADIPOSE TISSUE or the LIVER. A number of enzymes are involved in such lipid hydrolysis, such as LIPASE and LIPOPROTEIN LIPASE from various tissues.
The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.
Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
The time period before the development of symptomatic diabetes. For example, certain risk factors can be observed in subjects who subsequently develop INSULIN RESISTANCE as in type 2 diabetes (DIABETES MELLITUS, TYPE 2).
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
A collection of heterogenous conditions resulting from defective LIPID METABOLISM and characterized by ADIPOSE TISSUE atrophy. Often there is redistribution of body fat resulting in peripheral fat wasting and central adiposity. They include generalized, localized, congenital, and acquired lipodystrophy.
Insulin that has been modified to contain an ASPARTIC ACID instead of a PROLINE at position 38 of the B-chain.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.
An intermediate-acting INSULIN preparation with onset time of 2 hours and duration of 24 hours. It is produced by crystallizing ZINC-insulin-PROTAMINES at neutral pH 7. Thus it is called neutral protamine Hagedorn for inventor Hans Christian Hagedorn.
Fatty tissue under the SKIN through out the body.
Hormones released from neoplasms or from other cells that are not the usual sources of hormones.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A circumscribed melanosis consisting of a brown-pigmented, velvety verrucosity or fine papillomatosis appearing in the axillae and other body folds. It occurs in association with endocrine disorders, underlying malignancy, administration of certain drugs, or as in inherited disorder.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Regular course of eating and drinking adopted by a person or animal.
Fatty tissue composed of WHITE ADIPOCYTES and generally found directly under the skin (SUBCUTANEOUS FAT) and around the internal organs (ABDOMINAL FAT). It has less vascularization and less coloration than the BROWN FAT. White fat provides heat insulation, mechanical cushion, and source of energy.
Generic term for diseases caused by an abnormal metabolic process. It can be congenital due to inherited enzyme abnormality (METABOLISM, INBORN ERRORS) or acquired due to disease of an endocrine organ or failure of a metabolically important organ such as the liver. (Stedman, 26th ed)
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
Carbohydrates present in food comprising digestible sugars and starches and indigestible cellulose and other dietary fibers. The former are the major source of energy. The sugars are in beet and cane sugar, fruits, honey, sweet corn, corn syrup, milk and milk products, etc.; the starches are in cereal grains, legumes (FABACEAE), tubers, etc. (From Claudio & Lagua, Nutrition and Diet Therapy Dictionary, 3d ed, p32, p277)
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Nonsusceptibility of bacteria to the action of TETRACYCLINE which inhibits aminoacyl-tRNA binding to the 30S ribosomal subunit during protein synthesis.
Established cell cultures that have the potential to propagate indefinitely.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
Peptide hormones that cause an increase in the absorption of GLUCOSE by cells within organs such as LIVER, MUSCLE and ADIPOSE TISSUE. During normal metabolism insulins are produced by the PANCREATIC BETA CELLS in response to increased GLUCOSE. Natural and chemically-modified forms of insulin are also used in the treatment of GLUCOSE METABOLISM DISORDERS such as DIABETES MELLITUS.
The time frame after a meal or FOOD INTAKE.
Minor hemoglobin components of human erythrocytes designated A1a, A1b, and A1c. Hemoglobin A1c is most important since its sugar moiety is glucose covalently bound to the terminal amino acid of the beta chain. Since normal glycohemoglobin concentrations exclude marked blood glucose fluctuations over the preceding three to four weeks, the concentration of glycosylated hemoglobin A is a more reliable index of the blood sugar average over a long period of time.
The consumption of edible substances.
A nuclear transcription factor. Heterodimerization with RETINOID X RECEPTOR ALPHA is important in regulation of GLUCOSE metabolism and CELL GROWTH PROCESSES. It is a target of THIAZOLIDINEDIONES for control of DIABETES MELLITUS.
The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.
The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
A condition of elevated levels of TRIGLYCERIDES in the blood.
Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with LONGITUDINAL STUDIES which are followed over a period of time.
A well-characterized basic peptide believed to be secreted by the liver and to circulate in the blood. It has growth-regulating, insulin-like, and mitogenic activities. This growth factor has a major, but not absolute, dependence on GROWTH HORMONE. It is believed to be mainly active in adults in contrast to INSULIN-LIKE GROWTH FACTOR II, which is a major fetal growth factor.
Biosynthesis of GLUCOSE from nonhexose or non-carbohydrate precursors, such as LACTATE; PYRUVATE; ALANINE; and GLYCEROL.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
Diseases of plants.
Nonsusceptibility of an organism to the action of penicillins.
Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.
Regular insulin preparations that contain the HUMAN insulin peptide sequence.
Conditions with excess LIPIDS in the blood.
A condition caused by the excessive secretion of ANDROGENS from the ADRENAL CORTEX; the OVARIES; or the TESTES. The clinical significance in males is negligible. In women, the common manifestations are HIRSUTISM and VIRILISM as seen in patients with POLYCYSTIC OVARY SYNDROME and ADRENOCORTICAL HYPERFUNCTION.
Salts and esters of the 16-carbon saturated monocarboxylic acid--palmitic acid.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
Fatty tissue in the region of the ABDOMEN. It includes the ABDOMINAL SUBCUTANEOUS FAT and the INTRA-ABDOMINAL FAT.
Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.
The rate dynamics in chemical or physical systems.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
The ability of fungi to resist or to become tolerant to chemotherapeutic agents, antifungal agents, or antibiotics. This resistance may be acquired through gene mutation.
A syndrome of abnormally low BLOOD GLUCOSE level. Clinical hypoglycemia has diverse etiologies. Severe hypoglycemia eventually lead to glucose deprivation of the CENTRAL NERVOUS SYSTEM resulting in HUNGER; SWEATING; PARESTHESIA; impaired mental function; SEIZURES; COMA; and even DEATH.
Physiologically, the opposition to flow of air caused by the forces of friction. As a part of pulmonary function testing, it is the ratio of driving pressure to the rate of air flow.
Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.
A type of strength-building exercise program that requires the body muscle to exert a force against some form of resistance, such as weight, stretch bands, water, or immovable objects. Resistance exercise is a combination of static and dynamic contractions involving shortening and lengthening of skeletal muscles.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
A common saturated fatty acid found in fats and waxes including olive oil, palm oil, and body lipids.
Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.
Decrease in existing BODY WEIGHT.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen.
A state of insufficient flesh on the body usually defined as having a body weight less than skeletal and physical standards. Depending on age, sex, and genetic background, a BODY MASS INDEX of less than 18.5 is considered as underweight.
Increase in BODY WEIGHT over existing weight.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
A status with BODY WEIGHT that is above certain standard of acceptable or desirable weight. In the scale of BODY MASS INDEX, overweight is defined as having a BMI of 25.0-29.9 kg/m2. Overweight may or may not be due to increases in body fat (ADIPOSE TISSUE), hence overweight does not equal "over fat".
Procedures for finding the mathematical function which best describes the relationship between a dependent variable and one or more independent variables. In linear regression (see LINEAR MODELS) the relationship is constrained to be a straight line and LEAST-SQUARES ANALYSIS is used to determine the best fit. In logistic regression (see LOGISTIC MODELS) the dependent variable is qualitative rather than continuously variable and LIKELIHOOD FUNCTIONS are used to find the best relationship. In multiple regression, the dependent variable is considered to depend on more than a single independent variable.
The physical characteristics of the body, including the mode of performance of functions, the activity of metabolic processes, the manner and degree of reactions to stimuli, and power of resistance to the attack of pathogenic organisms.
An enzyme that catalyzes the transfer of D-glucose from UDPglucose into 1,4-alpha-D-glucosyl chains. EC
Pathological conditions in which the BLOOD GLUCOSE cannot be maintained within the normal range, such as in HYPOGLYCEMIA and HYPERGLYCEMIA. Etiology of these disorders varies. Plasma glucose concentration is critical to survival for it is the predominant fuel for the CENTRAL NERVOUS SYSTEM.
A plasma protein that circulates in increased amounts during inflammation and after tissue damage.
A condition of having excess fat in the abdomen. Abdominal obesity is typically defined as waist circumferences of 40 inches or more in men and 35 inches or more in women. Abdominal obesity raises the risk of developing disorders, such as diabetes, hypertension and METABOLIC SYNDROME X.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Nonsusceptibility of bacteria to the action of the beta-lactam antibiotics. Mechanisms responsible for beta-lactam resistance may be degradation of antibiotics by BETA-LACTAMASES, failure of antibiotics to penetrate, or low-affinity binding of antibiotics to targets.
Proteins found in any species of bacterium.
A subtype of non-receptor protein tyrosine phosphatases that includes two distinctive targeting motifs; an N-terminal motif specific for the INSULIN RECEPTOR, and a C-terminal motif specific for the SH3 domain containing proteins. This subtype includes a hydrophobic domain which localizes it to the ENDOPLASMIC RETICULUM.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
The technique that deals with the measurement of the size, weight, and proportions of the human or other primate body.
Cell surface receptors for ADIPONECTIN, an antidiabetic hormone secreted by ADIPOCYTES. Adiponectin receptors are membrane proteins with multiple cytoplasmic and extracellular regions. They are about 43 kDa and encoded by at least two genes with different affinities for globular and full-length adiponectin.
Physical activity which is usually regular and done with the intention of improving or maintaining PHYSICAL FITNESS or HEALTH. Contrast with PHYSICAL EXERTION which is concerned largely with the physiologic and metabolic response to energy expenditure.
A nodular organ in the ABDOMEN that contains a mixture of ENDOCRINE GLANDS and EXOCRINE GLANDS. The small endocrine portion consists of the ISLETS OF LANGERHANS secreting a number of hormones into the blood stream. The large exocrine portion (EXOCRINE PANCREAS) is a compound acinar gland that secretes several digestive enzymes into the pancreatic ductal system that empties into the DUODENUM.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
The measurement around the body at the level of the ABDOMEN and just above the hip bone. The measurement is usually taken immediately after exhalation.
Deposits of ADIPOSE TISSUE throughout the body. The pattern of fat deposits in the body regions is an indicator of health status. Excess ABDOMINAL FAT increases health risks more than excess fat around the hips or thighs, therefore, WAIST-HIP RATIO is often used to determine health risks.
A peptide of 36 or 37 amino acids that is derived from PROGLUCAGON and mainly produced by the INTESTINAL L CELLS. GLP-1(1-37 or 1-36) is further N-terminally truncated resulting in GLP-1(7-37) or GLP-1-(7-36) which can be amidated. These GLP-1 peptides are known to enhance glucose-dependent INSULIN release, suppress GLUCAGON release and gastric emptying, lower BLOOD GLUCOSE, and reduce food intake.
Insulin derivatives and preparations that are designed to induce a rapid HYPOGLYCEMIC EFFECT.
De novo fat synthesis in the body. This includes the synthetic processes of FATTY ACIDS and subsequent TRIGLYCERIDES in the LIVER and the ADIPOSE TISSUE. Lipogenesis is regulated by numerous factors, including nutritional, hormonal, and genetic elements.
Diabetes mellitus induced by PREGNANCY but resolved at the end of pregnancy. It does not include previously diagnosed diabetics who become pregnant (PREGNANCY IN DIABETICS). Gestational diabetes usually develops in late pregnancy when insulin antagonistic hormones peaks leading to INSULIN RESISTANCE; GLUCOSE INTOLERANCE; and HYPERGLYCEMIA.
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
Mitochondria of skeletal and smooth muscle. It does not include myocardial mitochondria for which MITOCHONDRIA, HEART is available.
Total number of calories taken in daily whether ingested or by parenteral routes.
Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics.
Benzopyrans saturated in the 2 and 3 positions.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).
The condition of weighing two, three, or more times the ideal weight, so called because it is associated with many serious and life-threatening disorders. In the BODY MASS INDEX, morbid obesity is defined as having a BMI greater than 40.0 kg/m2.
The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.
Fatty tissue under the SKIN in the region of the ABDOMEN.
The waist circumference measurement divided by the hip circumference measurement. For both men and women, a waist-to-hip ratio (WHR) of 1.0 or higher is considered "at risk" for undesirable health consequences, such as heart disease and ailments associated with OVERWEIGHT. A healthy WHR is 0.90 or less for men, and 0.80 or less for women. (National Center for Chronic Disease Prevention and Health Promotion, 2004)
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
Large, multinucleate single cells, either cylindrical or prismatic in shape, that form the basic unit of SKELETAL MUSCLE. They consist of MYOFIBRILS enclosed within and attached to the SARCOLEMMA. They are derived from the fusion of skeletal myoblasts (MYOBLASTS, SKELETAL) into a syncytium, followed by differentiation.
Intracellular signaling protein kinases that play a signaling role in the regulation of cellular energy metabolism. Their activity largely depends upon the concentration of cellular AMP which is increased under conditions of low energy or metabolic stress. AMP-activated protein kinases modify enzymes involved in LIPID METABOLISM, which in turn provide substrates needed to convert AMP into ATP.
Statistical models in which the value of a parameter for a given value of a factor is assumed to be equal to a + bx, where a and b are constants. The models predict a linear regression.
An enzyme that catalyzes the formation of nicotinamide mononucleotide (NMN) from nicotinamide and 5-phosphoribosyl-1-pyrophosphate, the rate-limiting step in the biosynthesis of the NAD coenzyme. It is also known as a growth factor for early B-LYMPHOCYTES, or an ADIPOKINE with insulin-mimetic effects (visfatin).
Transport proteins that carry specific substances in the blood or across cell membranes.
Contractile tissue that produces movement in animals.
A class of plasmids that transfer antibiotic resistance from one bacterium to another by conjugation.

Microvascular function relates to insulin sensitivity and blood pressure in normal subjects. (1/9934)

BACKGROUND: A strong but presently unexplained inverse association between blood pressure and insulin sensitivity has been reported. Microvascular vasodilator capacity may be a common antecedent linking insulin sensitivity to blood pressure. To test this hypothesis, we studied 18 normotensive and glucose-tolerant subjects showing a wide range in insulin sensitivity as assessed with the hyperinsulinemic, euglycemic clamp technique. METHODS AND RESULTS: Blood pressure was measured by 24-hour ambulatory blood pressure monitoring. Videomicroscopy was used to measure skin capillary density and capillary recruitment after arterial occlusion. Skin blood flow responses after iontophoresis of acetylcholine and sodium nitroprusside were evaluated by laser Doppler flowmetry. Insulin sensitivity correlated with 24-hour systolic blood pressure (24-hour SBP; r=-0.50, P<0.05). Capillary recruitment and acetylcholine-mediated vasodilatation were strongly and positively related to insulin sensitivity (r=0.84, P<0.001; r=0.78, P<0.001, respectively), and capillary recruitment was inversely related to 24-hour SBP (r=-0.53, P<0.05). Waist-to-hip ratio showed strong associations with insulin sensitivity, blood pressure, and the measures of microvascular function but did not confound the associations between these variables. Subsequent regression analysis showed that the association between insulin sensitivity and blood pressure was not independent of the estimates of microvascular function, and part of the variation in both blood pressure (R2=38%) and insulin sensitivity (R2=71%) could be explained by microvascular function. CONCLUSIONS: Insulin sensitivity and blood pressure are associated well within the physiological range. Microvascular function strongly relates to both, consistent with a central role in linking these variables.  (+info)

The treatment of insulin resistance does not improve adrenal cytochrome P450c17alpha enzyme dysregulation in polycystic ovary syndrome. (2/9934)

OBJECTIVE: To determine whether metformin. when given to non-diabetic women with polycystic ovary syndrome (PCOS), results in a reduction of insulin resistance and hyperinsulinemia while body weight is maintained. Also we aimed to see whether the reduction in insulin levels attenuates the activity of adrenal P450c17alpha enzyme in patients with PCOS. DESIGN: We investigated the 17-hydroxyprogesterone (17-OHP) and androstenedione responses to ACTH, insulin responses to an oral glucose tolerance test (OGTT) and glucose disposal rate in an insulin tolerance test before and after metformin therapy (500 mg, orally, twice daily, for 12 weeks). METHODS: The presence of hyperinsulinemia in 15 women with PCOS was demonstrated by an OGTT and results were compared with those of 10 healthy women. Insulin sensitivity was measured by the rate of endogenous glucose disposal after i.v. bolus injection of insulin. 17-OHP and androstenedione responses to ACTH were measured in all the women with PCOS and the normal women. RESULTS: Women with PCOS were hyperinsulinemic (102.0+/-13.0 (S.E.M.) VS 46.2+/-4.4 pmol/l) and hyperandrogenemic (free testosterone 15.3+/-1.7 vs 7.9+/-0.6 nmol/l; androstenedione 11.8+/-0.8 vs 8.2+/-0.6 nmol/l) and more hirsute (modified Ferriman-Gallwey score, 17.7+/-1.6 vs 3.0+/-0.3) than healthy women. In addition, women with PCOS had higher 17-OHP and androstenedione responses to ACTH when compared with healthy women. Metformin therapy resulted in some improvement in insulin sensitivity and reduced the basal and post-glucose load insulin levels. But 17-OHP and androstenedione responses to ACTH were unaltered in response to metformin. CONCLUSIONS: PCOS is characterized by hyperactivity of the adrenal P450c17alpha enzyme and insulin resistance. It seems that there is no direct relationship between insulin resistance and adrenal P450c17alpha enzyme dysregulation.  (+info)

No association between the -308 polymorphism in the tumour necrosis factor alpha (TNFalpha) promoter region and polycystic ovaries. (3/9934)

The tumour necrosis factor (TNF)2 allele appears to be linked with increased insulin resistance and obesity, conditions often found in overweight patients with polycystic ovary syndrome (PCOS). The significance of TNFalpha polymorphism in relation to the clinical and biochemical parameters associated with PCOS was investigated in 122 well-characterized patients with polycystic ovaries (PCO). Of these, 84 had an abnormal menstrual cycle and were classified as having PCOS, while the remaining 38 had a normal menstrual cycle and were classified as having PCO. There were a further 28 individuals without PCO (non-PCO) and 108 individuals whose PCO status was undetermined (reference population). The promoter region of the TNFalpha gene was amplified by polymerase chain reaction (PCR), and the presence or absence of the polymorphism at -308 was determined by single-strand conformational polymorphism (SSCP) analysis. The less common TNF allele (TNF2) was found as TNF1/2 or TNF2/2 in 11/38 (29%) of PCO subjects, 25/84 (30%) of PCOS subjects, 7/28 (25%) of non-PCO subjects, and 45/108 (42%) of the reference population. There was no significant difference in the incidence of the TNF2 allele between the groups. The relationship of TNF genotype to clinical and biochemical parameters was examined. In both the PCO group and the PCOS group, the presence of the TNF2 allele was significantly associated with lower glucose values obtained from the glucose tolerance testing (P<0.05). The TNF genotype was not significantly associated with any clinical or biochemical parameter measured in the PCO, PCOS or non-PCOS groups. Thus, the TNFalpha -308 polymorphism does not appear to strongly influence genetic susceptibility to polycystic ovaries.  (+info)

Training in swimming reduces blood pressure and increases muscle glucose transport activity as well as GLUT4 contents in stroke-prone spontaneously hypertensive rats. (4/9934)

Exercise improves muscle insulin sensitivity and GLUT4 contents. We investigated the beneficial effects of swimming training on insulin sensitivity and genetic hypertension using stroke-prone hypertensive rats (SHRSP). We studied the relationship between genetic hypertension and insulin resistance in SHRSP and Wistar Kyoto rats (WKY) as a control. The systolic blood pressure of SHRSP was significantly reduced by 4-week swimming training (208.4 +/- 6.8 mmHg vs. 187.2 +/- 4.1 mmHg, p < 0.05). The swimming training also resulted in an approximately 20% increase in the insulin-stimulated glucose transport activity (p < 0.05) of soleus muscle strips and an approximately 3-fold increase in the plasma membrane GLUT4 protein expression (p < 0.01) in SHRSP. However, basal and insulin-stimulated glucose transport activity and GLUT4 contents were not significantly different between WKY and SHRSP. There was no difference in insulin resistance in skeletal muscle of SHRSP as compared with WKY. Our results indicated swimming training exercise improved not only hypertension but also muscle insulin sensitivity and GLUT4 protein expression in SHRSP.  (+info)

Increased insulin sensitivity and obesity resistance in mice lacking the protein tyrosine phosphatase-1B gene. (5/9934)

Protein tyrosine phosphatase-1B (PTP-1B) has been implicated in the negative regulation of insulin signaling. Disruption of the mouse homolog of the gene encoding PTP-1B yielded healthy mice that, in the fed state, had blood glucose concentrations that were slightly lower and concentrations of circulating insulin that were one-half those of their PTP-1B+/+ littermates. The enhanced insulin sensitivity of the PTP-1B-/- mice was also evident in glucose and insulin tolerance tests. The PTP-1B-/- mice showed increased phosphorylation of the insulin receptor in liver and muscle tissue after insulin injection in comparison to PTP-1B+/+ mice. On a high-fat diet, the PTP-1B-/- and PTP-1B+/- mice were resistant to weight gain and remained insulin sensitive, whereas the PTP-1B+/+ mice rapidly gained weight and became insulin resistant. These results demonstrate that PTP-1B has a major role in modulating both insulin sensitivity and fuel metabolism, thereby establishing it as a potential therapeutic target in the treatment of type 2 diabetes and obesity.  (+info)

Insulin resistance of muscle glucose transport in male and female rats fed a high-sucrose diet. (6/9934)

It has been reported that, unlike high-fat diets, high-sucrose diets cause insulin resistance in the absence of an increase in visceral fat and that the insulin resistance develops only in male rats. This study was done to 1) determine if isolated muscles of rats fed a high-sucrose diet are resistant to stimulation of glucose transport when studied in vitro and 2) obtain information regarding how the effects of high-sucrose and high-fat diets on muscle insulin resistance differ. We found that, compared with rat chow, semipurified high-sucrose and high-starch diets both caused increased visceral fat accumulation and insulin resistance of skeletal muscle glucose transport. Insulin responsiveness of 2-deoxyglucose (2-DG) transport measured in epitrochlearis and soleus muscles in vitro was decreased approximately 40% (P < 0.01) in both male and female rats fed a high-sucrose compared with a chow diet. The high-sucrose diet also caused resistance of muscle glucose transport to stimulation by contractions. There was a highly significant negative correlation between stimulated muscle 2-DG transport and visceral fat mass. In view of these results, the differences in insulin action in vivo observed by others in rats fed isocaloric high-sucrose and high-starch diets must be due to additional, specific effects of sucrose that do not carry over in muscles studied in vitro. We conclude that, compared with rat chow, semipurified high-sucrose and high-cornstarch diets, like high-fat diets, cause increased visceral fat accumulation and severe resistance of skeletal muscle glucose transport to stimulation by insulin and contractions.  (+info)

Relationship of plasmin generation to cardiovascular disease risk factors in elderly men and women. (7/9934)

Plasmin-alpha2-antiplasmin complex (PAP) marks plasmin generation and fibrinolytic balance. We recently observed that elevated levels of PAP predict acute myocardial infarction in the elderly, yet little is known about the correlates of PAP. We measured PAP in 800 elderly subjects who were free of clinical cardiovascular disease in 2 cohort studies: the Cardiovascular Health Study and the Honolulu Heart Program. Median PAP levels did not differ between the Cardiovascular Health Study (6.05+/-1.46 nmol/L) and the Honolulu Heart Program (6.11+/-1.44 nmol/L), and correlates of PAP were similar in both cohorts. In CHS, PAP levels increased with age (r=0. 30), procoagulant factors (eg, factor VIIc, r=0.15), thrombin activity (prothrombin fragment F1+2, r=0.29), and inflammation-sensitive proteins (eg, fibrinogen, r=0.44; factor VIIIc, r=0.37). PAP was associated with increased atherosclerosis as measured by the ankle-arm index (AAI) (P for trend, +info)

Relative contribution of insulin and its precursors to fibrinogen and PAI-1 in a large population with different states of glucose tolerance. The Insulin Resistance Atherosclerosis Study (IRAS). (8/9934)

Hyperinsulinemia is associated with the development of coronary heart disease. However, the underlying mechanisms are still poorly understood. Hypercoagulability and impaired fibrinolysis are possible candidates linking hyperinsulinism with atherosclerotic disease, and it has been suggested that proinsulin rather than insulin is the crucial pathophysiological agent. The aim of this study was to investigate the relationship of insulin and its precursors to markers of coagulation and fibrinolysis in a large triethnic population. A strong and independent relationship between plasminogen activator inhibitor-1 (PAI-1) antigen and insulin and its precursors (proinsulin, 32-33 split proinsulin) was found consistently across varying states of glucose tolerance (PAI-1 versus fasting insulin [proinsulin], r=0.38 [r=0.34] in normal glucose tolerance; r=0.42 [r=0.43] in impaired glucose tolerance; and r=0.38 [r=0.26] in type 2 diabetes; all P<0.001). The relationship remained highly significant even after accounting for insulin sensitivity as measured by a frequently sampled intravenous glucose tolerance test. In a stepwise multiple regression model after adjusting for age, sex, ethnicity, and clinic, both insulin and its precursors were significantly associated with PAI-1 levels. The relationship between fibrinogen and insulin and its precursors was significant in the overall population (r=0.20 for insulin and proinsulin; each P<0.001) but showed a more inconsistent pattern in subgroup analysis and after adjustments for demographic and metabolic variables. Stepwise multiple regression analysis showed that proinsulin (split products) but not fasting insulin significantly contributed to fibrinogen levels after adjustment for age, sex, clinic, and ethnicity. Decreased insulin sensitivity was independently associated with higher PAI-1 and fibrinogen levels. In summary, we were able to demonstrate an independent relationship of 2 crucial factors of hemostasis, fibrinogen and PAI-1, to insulin and its precursors. These findings may have important clinical implications in the risk assessment and prevention of macrovascular disease, not only in patients with overt diabetes but also in nondiabetic subjects who are hyperinsulinemic.  (+info)

BACKGROUND: Metabolic Syndrome (MS) is prevalant in China, especially according to the pediatric obesity group. Based on the MS-CHN2012 definition for Chinese children and adolescents the need to explore and establish a convienent MS screening become imminent. This study aims to investigate the optimal cut-off values, compare the accuracy for the (TriGlycerides (TG) to High-Density Lipoprotein Cholesterol (HDL-C)) (TG/HDL-C) ratio and Homeostasis Model Assessment Insulin Resistance (HOMA-IR) indexs to identify Metabolic Syndrome in obese pediatric population in China.. METHOD: A total sample of 976 children (female 286 male 690, BMI , = 95 percentile) aged from 6-16 years underwent a medical assessment including a physical examination and investigations of total cholesterol, high-density lipoprotein, low-density lipoprotein, triglycerides, insulin, glucose, and oral glucose tolerance test to identify the components of Metabolic Syndrome. The validity and accuracy between TG/HDL-C ratio and ...
OBJECTIVE: Several methods have been proposed to evaluate insulin sensitivity from the data obtained from the oral glucose tolerance test (OGTT). However, the validity of these indices has not been rigorously evaluated by comparing them with the direct measurement of insulin sensitivity obtained with the euglycemic insulin clamp technique. In this study, we compare various insulin sensitivity indices derived from the OGTT with whole-body insulin sensitivity measured by the euglycemic insulin clamp technique. RESEARCH DESIGN AND METHODS: In this study, 153 subjects (66 men and 87 women, aged 18-71 years, BMI 20-65 kg/m2) with varying degrees of glucose tolerance (62 subjects with normal glucose tolerance, 31 subjects with impaired glucose tolerance, and 60 subjects with type 2 diabetes) were studied. After a 10-h overnight fast, all subjects underwent, in random order, a 75-g OGTT and a euglycemic insulin clamp, which was performed with the infusion of [3-3H]glucose. The indices of insulin ...
TY - JOUR. T1 - The association of SNP276G,T at adiponectin gene with circulating adiponectin and insulin resistance in response to mild weight loss. AU - Shin, M. J.. AU - Jang, Y.. AU - Koh, S. J.. AU - Chae, J. S.. AU - Kim, O. Y.. AU - Lee, J. E.. AU - Ordovas, J. M.. AU - Lee, J. H.. PY - 2006/12/21. Y1 - 2006/12/21. N2 - Objective:The purpose of this study was to determine whether common single nucleotide polymorphisms (SNPs) at the adiponectin (ADIPOQ) locus influence changes in circulating adiponectin and the features of insulin resistance in response to a weight loss intervention.Subjects:In total, 294 nondiabetic/overweight-obese Koreans participated in a clinical intervention study lasting 12 weeks involving a caloric reduction of -300kcal/day.Methods: Plasma adiponectin, blood lipids, glucose and insulin concentrations were measured at baseline and after weight loss. Insulin resistance was estimated by homeostasis model assessment insulin resistance (HOMA-IR) derived from fasting ...
TY - JOUR. T1 - Skeletal muscle insulin resistance. T2 - the interplay of local lipid excess and mitochondrial dysfunction. AU - Chow, Lisa S. AU - From, Arthur H. AU - Seaquist, Elizabeth R. PY - 2010/1. Y1 - 2010/1. N2 - This review explores the complex relationship between excess lipid exposure, mitochondrial dysfunction, and insulin resistance at the level of human skeletal muscle. Lipotoxicity, that is, the elevation of lipids and/or associated lipid metabolites within blood and tissues with subsequent metabolic derangement, has been proposed as a possible mechanism of skeletal muscle insulin resistance. Intravenous lipid infusion is a well-documented method of inducing insulin resistance. Although IMCL content has been correlated with insulin resistance, there is increasing evidence that lipid metabolites such as 4-HNE, DAG, ceramide, and LC-CoA may play a more significant role than TGs in producing skeletal muscle insulin resistance. The association between mitochondrial dysfunction and ...
Duncan, E, Walker, SJ, Ezzat, V, Wheatcroft, S, Li, J-M, Shah, A and Keamey, M (2006) Mild whole body insulin resistance and accelerated endothelial dysfunction: Increased reactive oxygen species derived from mitochondria during ageing despite preserved glycaemic control In: 79th Annual Scientific Session of the American-Heart-Association, 2006-11-12 - 2006-11-15, Chicago, IL. Full text not available from this repository ...
TY - JOUR. T1 - Adipose-Resident Group 1 Innate Lymphoid Cells Promote Obesity-Associated Insulin Resistance. AU - OSullivan, Timothy E.. AU - Rapp, Moritz. AU - Fan, Xiying. AU - Weizman, Orr El. AU - Bhardwaj, Priya. AU - Adams, Nicholas M.. AU - Walzer, Thierry. AU - Dannenberg, Andrew J.. AU - Sun, Joseph C.. PY - 2016. Y1 - 2016. N2 - Innate lymphoid cells (ILCs) function to protect epithelial barriers against pathogens and maintain tissue homeostasis in both barrier and non-barrier tissues. Here, utilizing Eomes reporter mice, we identify a subset of adipose group 1 ILC (ILC1) and demonstrate a role for these cells in metabolic disease. Adipose ILC1s were dependent on the transcription factors Nfil3 and T-bet but phenotypically and functionally distinct from adipose mature natural killer (NK) and immature NK cells. Analysis of parabiotic mice revealed that adipose ILC1s maintained long-term tissue residency. Diet-induced obesity drove early production of interleukin (IL)-12 in adipose ...
This trial is entitled "Bumetanide has a more favourable effect on insulin resistance than furosemide in patients with heart failure - a pilot study".
TY - JOUR. T1 - Dissociation between metabolic and vascular insulin resistance in aging. AU - Schulman, Ivonne Hernandez. AU - Zhou, Ming Sheng. AU - Jaimes, Edgar A.. AU - Raij, Leopoldo. PY - 2007/7. Y1 - 2007/7. N2 - Physiological actions of insulin via activation of the phosphatidylinositol 3-kinase/Akt pathway in the endothelium serve to couple regulation of hemodynamic and metabolic homeostasis. Insulin resistance, endothelial dysfunction, and hypertension increase in prevalence with aging. We investigated the metabolic and endothelial actions of insulin in 24- vs. 3-mo Sprague-Dawley rats. With the use of the hyperinsulinemic euglycemic clamp, the rate of glucose infusion necessary to maintain equivalent plasma glucose (5.5 mmol/l) was similar in 24- vs. 3-mo rats, as was fasting glucose (5.2 ± 0.33 vs. 4.4 ± 0.37 mmol/l; mean ± SE) and insulin (0.862 ± 0.193 vs. 1.307 ± 0.230 mg/l). Systolic blood pressure was higher in 24-mo rats (133 ± 5 vs. 110 ± 4 mmHg; P = 0.005). Endothelial ...
Researchers at the University of California, San Diego, School of Medicine have identified a particular subset of cells that are linked to obesity-associated insulin resistance, and that offer a promising new target for the treatment of diabetes. They showed that depletion of these cells, called CD11c-positive, in obese mice resulted in a reversal of obesity-associated insulin resistance.
Zhu, Caihong; Schwarz, Petra; Abakumova, Irina; Aguzzi, Adriano (2015). Unaltered prion pathogenesis in a mouse model of high-fat diet-induced insulin resistance. PLoS ONE, 10(12):e0144983. ...
View more ,Abstract: Insulin resistance ensues when normal physiological concentrations of insulin are unable to induce effective cellular insulin signalling and glucose uptake by insulin sensitive tissues. It is caused by several abnormalities that include; 1) an overabundance of circulating free fatty acids (and dyslipidaemia), 2) systemic inflammation caused by increased tissue and circulating pro-inflammatory cytokines, and, 3) over activation of the systemic and organ specific renin-angiotensin systems. Although usually associated with obesity, insulin resistance is not a condition that only afflicts obese individuals. Dyslipidaemia which is implicated in the aetiology of insulin resistance can be caused by adipose tissue expansion (obesity) or the increased consumption of lipogenic fructose which has profound effects on liver metabolism and serum lipid profiles. The primary reason fructose is implicated in insulin resistance is because it induces hepatic lipogenesis which would directly ...
In this issue of Circulation Research, Kim et al provide additional mechanistic insights into the link between obesity, innate immunity, vascular insulin resistance, and vascular inflammation in a murine model of high-fat diet-induced obesity.11 The authors induced obesity in C57BL6 mice by feeding them a high-fat diet for 8 weeks. Insulin signaling in aortic tissue from high-fat-fed mice was impaired, as measured by reduced phosphorylation of AKT and eNOS in response to insulin administration consistent with cellular evidence of insulin resistance. These effects on insulin resistance were associated with evidence of activation of NF-kB dependent inflammatory pathways, as indicated by increased phosphorylation of IKK-β and increased expression of the NF-κB dependent proinflammatory genes IL-6 and ICAM-1.. To further characterize the signaling pathway by which high-fat diet induces insulin resistance and proinflammatory vascular response, the authors did similar studies in TLR-4-null mice. ...
Michael Dube, for natap.org. Current dogma has early insulin resistance from ART blamed on protease inhibitors, and late insulin resistance attributed to lipoatrophy induced by nucleoside drugs. But studies in healthy subjects have suggested that at least some NRTIs may cause early insulin resistance as well.. The central finding presented by Marit van Vonderan from Amsterdam was that peripheral tissue insulin resistance (as measured by the gold standard hyperinsulinemic clamp procedure) occurred only occurred in subjects (all male) who initiated zidovudine-lamivudine plus Kaletra and not in those who received nevirapine plus Kaletra.. This ZDV-3TC associated insulin resistance was present at 3 months, a time point where limb fat was actually increased from baseline. At 24 months limb fat was down in the ZDV-3TC group, but this insulin resistance occurred well before limb fat had decreased, suggesting a more direct effect of the NRTI therapy. This data suggests that we need to pay attention to ...
Title: Myocardial Insulin Resistance and Cardiac Complications of Diabetes. VOLUME: 5 ISSUE: 2. Author(s):E. Dale Abel. Affiliation:Program in Human Molecular Biology and Genetics, Division of Endocrinology, Metabolism and Diabetes, University of Utah, 15 North 2030 East, Bldg. &# 533, Room 3410B, Salt Lake City, UT 84112, USA.. Keywords:insulin resistance, diabetes, obesity, myocardial energetics, cardiac hypertrophy, cardiac metabolism. Abstract: Cardiovascular disease is a major cause of mortality and morbidity in individuals with obesity, type 2 diabetes and the metabolic syndrome. The mechanisms for this are partially understood, but include increased atherosclerosis, hypercoagulability and increased hypertension. Epidemiological data suggests however, that a component of the excess cardiovascular mortality occurs independently of underlying coronary artery disease. Indeed, diabetes is an independent risk factor for the development of heart failure and the mechanisms responsible remain to ...
Aim Increased frequency of cardiovascular disease and its possible relations with insulin resistance have been reported in patients with inflammatory diseases. The aim of our study was to investigate insulin resistance and serum adiponectin levels as cardiovascular risk markers in patients with Behçets disease.. Method Study population consisted of 40 patients with Behçets disease (BD) and a control group composed of age, gender, body mass index-matched 46 healthy individuals. All patients were examined for signs of Behçets disease. Body mass index, waist and hip circumference were measured. Insulin resistance was evaluated using the homeostasis model assessment-insulin resistance method. Erythrocyte sedimentation rate (ESR), lipid profile, high sensitive CRP (hsCRP), adiponectin, TNF-α, IL-6 and IL-8 levels were measured.. Results Erythrocyte sedimentation rate, serum hsCRP and IL-6 levels were significantly higher in patients with BD than those in the controls (P = 0.001, P = 0.001, P = ...
Fingerprint Dive into the research topics of Adipose tissue insulin resistance in youth on the spectrum from normal weight to obese and from normal glucose tolerance to impaired glucose tolerance to type 2 diabetes. Together they form a unique fingerprint. ...
Fingerprint Dive into the research topics of Role of adipose tissue insulin resistance in the natural history of type 2 diabetes: Results from the san antonio metabolism study. Together they form a unique fingerprint. ...
TY - JOUR. T1 - Membrane-targeted phosphatidylinositol 3-kinase mimics insulin actions and induces a state of cellular insulin resistance. AU - Egawa, Katsuya. AU - Sharma, Prem M.. AU - Nakashima, Naoki. AU - Huang, Yi. AU - Huver, Evana. AU - Boss, Gerry R.. AU - Olefsky, Jerrold M.. PY - 1999/5/14. Y1 - 1999/5/14. N2 - Phosphatidylinositol (PI) 3-kinase plays an important role in various insulin-stimulated biological responses including glucose transport, glycogen synthesis, and protein synthesis. However, the molecular link between PI 3- kinase and these biological responses is still unclear. We have investigated whether targeting of the catalytic p110 subunit of PI 3-kinase to cellular membranes is sufficient and necessary to induce PI 3-kinase dependent signaling responses, characteristic of insulin action. We overexpressed Myc- tagged, membrane-targeted p110 (p110(CAAX)), and wild-type p110 (p110(WT)) in 3T3-L1 adipocytes by adenovirus-mediated gene transfer. Overexpressed p110(CAAX) ...
We assessed whether insulin sensitivity improved after renal denervation (RDN) for resistant hypertension. Twenty-three patients underwent a two-step hyperinsulinemic euglycemic clamp (HEC) with glucose tracer and labeled glucose infusion and oral glucose tolerance test (OGTT) before and 6 months after RDN. Eighteen patients had metabolic syndrome at baseline. Blood pressure declined significantly after RDN whereas fasting plasma glucose (5.9 ± 0.7 mmol/L), insulin (254 (88-797) pmol/L), C- peptide (2.4 (0.9-5.7) nmol/L) remained unchanged. Endogenous glucose release during HEC was less suppressed after RDN, suggesting a slight decrease in hepatic insulin sensitivity. During high-dose insulin infusion, whole-body glucose disposal was low and remained unchanged after RDN, indicating persistent peripheral insulin resistance. Area under the curve 0-120min for glucose and insulin during OGTT, Quantitative Insulin Sensitivity Check Index, Simple Index assessing Insulin Sensitivity oral glucose ...
We previously have shown that during the transition from NGT to IGT to T2DM, β-cell function progressively declines and peripheral insulin resistance progressively increases (31,35). Adipo-IR also is increased in patients with T2DM, but the natural history of its development as individuals progress from NGT to IGT to T2DM has been poorly studied. As recently reviewed (21), a number of indices of adipocyte insulin resistance have been proposed that are based on tracer turnover (i.e., labeled palmitate or glycerol) or FFA suppression during insulin infusion (euglycemic-hyperinsulinemic clamp) or OGTT. In the current study, we used the product of fasting plasma FFA and fasting plasma insulin concentrations as the index of Adipo-IR. Because the circulating plasma FFA concentration closely reflects the rate of peripheral lipolysis, Adipo-IR represents an index for adipose tissue resistance to the antilipolytic effect of insulin. The hyperbolic relationship between plasma insulin and FFA ...
insulin resistance - MedHelps insulin resistance Center for Information, Symptoms, Resources, Treatments and Tools for insulin resistance. Find insulin resistance information, treatments for insulin resistance and insulin resistance symptoms.
Inflammation plays a key role in the development and progression of type-2 diabetes (T2D), a disease characterised by peripheral insulin resistance and systemic glucolipotoxicity. Visceral adipose tissue (AT) is the main source of inflammation early in disease course. Macrophages are innate immune cells that populate all peripheral tissues, including AT. Dysregulated AT macrophage (ATM) responses to microenvironmental changes are at the root of aberrant inflammation and development of insulin resistance, locally and systemically. The inflammatory activation of macrophages is regulated at multiple levels: cell surface receptor stimulation, intracellular signalling, transcriptionally and metabolically. This review will cover the main mechanisms involved in AT inflammation and insulin resistance in T2D. First, we will describe the physiological and pathological changes in AT that lead to inflammation and insu- lin resistance. We will next focus on the transcriptional and metabolic mechanisms described that
Similar to skeletal muscle, glucose utilization in adipose tissue also affects whole body glucose disposal. Following DEX treatment, a GR-dependent and transcription-independent mechanism that attenuates insulin signal has been identified recently in cultured adipocytes (107). The decreased insulin sensitivity was attributed to postreceptor signaling defects (156). Thus, incubation with DEX significantly inhibits total mRNA and tyrosine phosphorylation of IRS-1 (156, 181). The decreased IRS-1 reduces activation of phosphatidylinositol 3-kinase (PI 3-kinase), which plays a key role in the regulation of GLUT4 transport (156). Although the total amount of GLUT4 protein in 3T3-L1 adipocytes was unchanged, basal and insulin-induced transport of GLUT4 decreased following DEX (156). Total GLUT1 protein decreased in this experiment (156). Interestingly, even though IRS-1 and PI 3-kinase were normalized via IRS-1 overexpression, insulin-induced impairment of glucose uptake by DEX did not significantly ...
Many landmark studies have reported the Nod-like receptor proteins containing Pyrin domain (NLRP3) inflammasome activation in metabolic diseases that include obesity, atherosclerosis and type 2 diabetes. Therefore, the present study was aimed: (i) to determine the role of NLRP3 in inflammation and insulin resistance in high fat diet-induced obesity (DIO) model of mice, and (ii) to determine whether parthenolide, a NLRP3 inhibitor, is able to protect mice against inflammation and insulin resistance in high fat DIO model.. METHODS: Lipopolysaccharide (1 ng/ml) primed mouse intraperitoneal macrophages were treated with Parthenolide (0.1 to 30 μM) to evaluate its effect on TNF-α and IL-1β. Parthenolide and Pioglitazone were administered to DIO mice (fed 60% high fat diet) at 5 and 30 mg/kg QD, PO, respectively for 60 days to evaluate their effect on insulin resistance.. RESULTS: Parthenolide (5 mg/kg) markedly attenuated inflammatory cytokines as evidenced by significant and dose dependant ...
We found in a community-based cohort that insulin resistance, based on HOMA-IR, was associated with an increased risk of incident HF among those without diabetes at baseline. This risk appeared to occur at lower levels than the previously-defined insulin resistance threshold of a HOMA-IR of 2.5 and was not modified by race or BMI, but the relationship between insulin resistance and HF was stronger in younger participants, in females, and in those with lower baseline risk of HF. However, the association between insulin resistance and HF was no longer significant at HOMA-IR levels ≥2.5. Interim MI did not mediate the association between insulin resistance and HF.. The relationship between insulin resistance and incident HF has varied in prior studies. Our findings of a significant association between HOMA-IR, modeled flexibly with the use of cubic splines, and incident HF following adjustment for risk factors for HF corroborate a recent analysis of the Cardiovascular Health Study, which also ...
CONTEXT: The etiological mechanism of bile acid (BA) effects on insulin resistance and obesity is unknown. OBJECTIVE: To determine if plasma BA are elevated in human obesity and/or insulin resistance. DESIGN: Observational study. SETTING: Academic research center. PARTICIPANTS: 71 adult volunteers formed four groups: lean insulin-sensitive (BMI|/=25kg/m 2, HOMA-IR|2.0, n=19), overweight/obese non-diabetic who were either insulin-sensitive (Obsensitive, BMI|25kg/m 2, HOMA-IR|1.5, n=11), or insulin-resistant (Obresistant, BMI|25kg/m 2, HOMA-IR|3.0, n=20), and type 2 diabetes (T2D, n=21). MAIN OUTCOME MEASURES: Insulin sensitivity by hyperinsulinemic-euglycemic clamp, body composition by dual energy x-ray absorptiometry, abdominal fat distribution and liver density by CT and plasma BA. RESULTS: In the Obresistant group, glucose infusion rate/fat free mass (GIR/FFM, an inverse measure of insulin resistance) was significantly lower, and visceral and liver fat higher, compared to lean and Obsensitive subjects
Insulin resistance is defined as a disturbed metabolic response to exogenous or endogenous insulin. Insulin resistance results in increased insulin levels in blood plasma compared to those required for the available level of glucose. Chronic heart failure is currently one of the most severe and prognostically unfavorable cardiovascular diseases. Chronic heart failure is a progressive syndrome, and patients with asymptomatic CHF may proceed to a group of the most severely ill non-responders within 1-5 years. Insulin resistance may be present in CHF both as minimal changes (predisposition to hypo- or hyperglycemia; flattened glycemic curve) and as impaired resting glucose tolerance or DM. At present time, there is no unambiguous opinion on the correction of insulin resistance syndrome in patients with CHF. Considering the growing population of patients with DM and CHF, there is a need for a special (desirably randomized) trial to define an optimal antidiabetic therapy for patients with CHF and ...
Tumour necrosis factor alpha (TNF-α), acting as a modulator of gene expression in adipocytes, has been linked to the development of insulin resistance and obesity. The aim of this study was to investigate whether the A/G variation at position −308 in the TNFα promoter influences the body weight, insulin resistance, and postprandial lipaemia in Polish Caucasians. One hundred twenty one subjects, 38 men and 83 women, representing 40 obese families, were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). TNF-1 (GG) and TNF-2 (GA and AA) allele carriers were compared with respect to body mass index, fat/lean body mass composition, waist-to-hip ratio, as well as fasting lipids, glucose, leptin, and insulin fasting, and during the oral glucose tolerance test (4 points within 2 hours) and oral lipid tolerance test (OLTT; 5 points within 8 hours). The insulin sensitivity indices HOMA-IR (homeostasis model assessment of insulin resistance), ISI-COMP (whole ...
Prevalence of type 2 diabetes mellitus (T2DM) is increasing worldwide. To reduce its risk and progression, preventive strategies are needed. Vitamin supplementation such as vitamin D is one of the strategies. This study was designed to investigate the effect of injection of vitamin D on insulin resistance and anthropometric parameters in T2DM. This randomized double-blind clinical trial was conducted with 42 diabetic patients in two groups; intervention group with single intramuscular injection of 300,000 International Unit (IU) of vitamin D3 and the placebo group. After recording demographic and anthropometric factors (waist circumference, blood pressure and body mass index), fasting blood samples was taken for measurement of blood glucose, 25-hydroxyvitamin D3 (25-OHD3), insulin, glycosylated hemoglobin A1c (HbA1c) and estimation of Homeostasis Model Assessment Index (HOMA) in two times; before study and after three months. Two groups had similar baseline characteristics (each group = 21 subjects).
One study from China by Chen et al.[2] claimed that viral clearance is delayed by diabetes, hypertension, male gender (perhaps because the gene for ACE2 is on the X chromosome), and old age, which may worsen the prognosis of COVID-19 infection, likely due to the increased expression of ACE2. The authors recommended that the use of ACE inhibitors be carefully considered in such populations, as it may lead to upregulation of ACE2. However, there is another school of thought that ACE2 overexpression may help as it converts angiotensin-2 into angiotensin 1-7, which has effects exactly opposite to that of angiotensin-2, meaning that it can balance angiotensin-2 in the body so that it is potentially useful to protect against ARDS and the cytokine storm.[2] Therefore, ACE 2 seems to attract the virus into the pneumocytes, but on the contrary, perhaps also equips the cells against a cytokine storm. Thus, some authors have contended that blockage of the renin-angiotensin-aldosterone system (RAAS) by ACE ...
TY - JOUR. T1 - Unique Metabolic Features of Adults Discordant for Indices of Insulin Resistance. AU - Song, Yilin. AU - Søndergaard, Esben. AU - Jensen, Michael D.. N1 - Funding Information: Financial Support: This work was supported by the National. PY - 2020/6/9. Y1 - 2020/6/9. N2 - Purpose: Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) and Adipose Insulin Resistance index (ADIPO-IR) values are often concordant. In this study we evaluated whether there are groups discordant for HOMA-IR and ADIPOpalmitate-IR and, if so, what are their defining characteristics. Methods: The body composition, basal metabolic rate (BMR), fasting plasma lipids, insulin, glucose, and free fatty acid (FFA) palmitate concentrations data of 466 volunteers from previous research studies were abstracted and analyzed. The middle 2 population quartiles for HOMA-IR and Adipose Insulin Resistance index palmitate concentration (ADIPOpalmitate-IR) defined medium HOMA-IR and ADIPOpalmitate-IR (MH and MA), the ...
Pigment epithelium-derived factor (PEDF) is an anti-angiogenic, immunomodulatory, and neurotrophic serine protease inhibitor protein. PEDF is evolving as a novel metabolic regulatory protein that plays a causal role in insulin resistance. Insulin resistance is the central pathogenesis of metabolic disorders such as obesity, type 2 diabetes mellitus, polycystic ovarian disease, and metabolic syndrome, and PEDF is associated with them. The current evidence suggests that PEDF administration to animals induces insulin resistance, whereas neutralisation improves insulin sensitivity. Inflammation, lipolytic free fatty acid mobilisation, and mitochondrial dysfunction are the proposed mechanism of PEDF-mediated insulin resistance. This review summarises the probable mechanisms adopted by PEDF to induce insulin resistance, and identifies PEDF as a potential therapeutic target in ameliorating insulin resistance.. ...
The intestinal immune system is emerging as an important contributor to obesity-related insulin resistance, but the role of intestinal B cells in this context is unclear. Here, we show that high fat diet (HFD) feeding alters intestinal IgA+ immune cells and that IgA is a critical immune regulator of glucose homeostasis. Obese mice have fewer IgA+ immune cells and less secretory IgA and IgA-promoting immune mediators. HFD-fed IgA-deficient mice have dysfunctional glucose metabolism, a phenotype that can be recapitulated by adoptive transfer of intestinal-associated pan-B cells. Mechanistically, IgA is a crucial link that controls intestinal and adipose tissue inflammation, intestinal permeability, microbial encroachment and the composition of the intestinal microbiome during HFD. Current glucose-lowering therapies, including metformin, affect intestinal-related IgA+ B cell populations in mice, while bariatric surgery regimen alters the level of fecal secretory IgA in humans. These findings identify
New study finds the mechanism for insulin resistance leading to type 2 diabetes. Earlier work by Joshua Knowles, MD, PhD, an assistant professor of cardiovascular medicine at Stanford, and his team showed the connection of a human gene, NAT2, variant with insulin resistance in humans. The fact that type 2 diabetes was caused by insulin resistance was known to researchers for decades. However, the cause for this phenomenon was a mystery. Insulin, a hormone secreted by the pancreas, helps fat and muscle cells take up glucose from the blood. Insulin resistance is caused when human cells dont respond to insulin, resulting in the build up of glucose in the blood and subsequently leading to the production of even more insulin. Weve identified a mechanism for insulin resistance that involves a gene that ties insulin resistance to mitochondrial function, said Knowles. Scientists at the Stanford University School of Medicine and the University of Wisconsin have begun to find the connections between ...
Chronic heart failure (CHF) is associated with marked insulin resistance, characterized by both fasting and stimulated hyperinsulinemia. Furthermore, insulin resistance is a predictor of CHF and associated with more severe disease and a worse prognosis in patients with CHF. In CHF patients, therefore, insulin resistance is not merely a function of adiposity and may have implications in the pathophysiology of CHF disease progression. Angiotensin II negatively modulates insulin-mediated actions by regulating multiple levels of the insulin signaling cascade such as the insulin receptor, IRS, and PI3-kinase. Furthermore, both ACE inhibitors and angiotensin II receptor blockers (ARB) improve glycemic status not only in patients with type II diabetes but also in patients with hypertension and the metabolic syndrome. On the other hand, it is well known that some cytokines, such as TNF-α, are involved with pathophysiology of insulin resistance and CHF. However, it is still unclear whether the ARB ...
To our knowledge, this study is the first to show that a major protein-bound uremic toxin, PCS, induces insulin resistance in vivo in mice (Figure 2), as well as in vitro in C2C12 myotubes (Figure 6). The disruption of insulin signaling associated with CKD was described in 1955,32 and the effects of kidney disease on renal uptake and excretion of insulin were reported in 1970.33 Insulin resistance in CKD was evidenced by DeFronzo et al.17 using the gold standard euglycemic hyperinsulinemic clamp technique. In CKD, the decline of renal function is associated with the development of insulin resistance, and insulin resistance is recognized as an independent risk factor for cardiovascular morbidity and mortality in patients with CKD.19 However, the exact causes of insulin resistance in CKD are still poorly defined.20,22,23,34,35 McCaleb et al.36 demonstrated that isolated rat adipocytes had inhibition of insulin-stimulated glucose uptake after incubation with serum from patients with CKD, whereas ...
Obesity has reached epidemic proportions, but little is known about its influence on the intestinal immune system. Here we show that the gut immune system is altered during high-fat diet (HFD) feeding and is a functional regulator of obesity-related insulin resistance (IR) that can be exploited ther …
The effects of salicylates on insulin resistance. There is significant overlap between the intracellular events induced by TGs (or FFAs) and TNF regarding the mechanisms of insulin resistance. Both stimuli activate IKK-β and decrease insulin-induced tyrosine phosphorylation of IRS-1; both increase intracellular ceramide concentrations, which leads to inhibition of Akt/protein kinase B activation and inhibition of GLUT-4 translocation. These effects induce a state of insulin resistance. The effects of salicylate compounds on these pathways may be divergent. That is, they may improve insulin resistance by blocking the activation of IKK-β (top), or they may worsen insulin resistance by inhibiting PG synthesis and thus potentiating TNF release (bottom). In addition, inhibition of PG will decrease synthesis of leptin, which is known to improve insulin sensitivity by stimulating IRS-1-associated PI 3-kinase activity. The beneficial effect of leptin on insulin action is thus decreased (bottom ...
Insulin resistance is associated with increased circulating lipids and skeletal muscle lipid content. Chronic nicotinic acid (NA) treatment reduces insulin sensitivity and provides a model of insulin resistance. We hypothesized that the reduction in insulin sensitivity occurs via elevation of circulating nonesterified fatty acids (NEFAs) and an increase in intramyocellular lipid (IMCL). A total of 15 nondiabetic males (mean age 27.4 +/- 1.6 years) were treated with NA (500 mg daily for 1 week, 1 g daily for 1 week). Insulin sensitivity (glucose infusion rate [GIR]) was determined pre- and post-NA by euglycemic-hyperinsulinemic clamp. Substrate oxidation was determined by indirect calorimetry. Skeletal muscle lipid was assessed by estimation of long-chain acyl-CoA (LCACoA) and triglyceride (TG) content and by (1)H-magnetic resonance spectroscopy quantification of IMCL (n = 11). NA reduced GIR (P =.03) and nonoxidative glucose disposal (P ,.01) and increased fasting NEFAs (P =.01). The decrease in ...
Insulin resistance usually occurs early in the development of type 2 diabetes. An altered balance in the autonomic nervous system and in certain endocrine and inflammatory pathways, might contribute to the development of insulin resistance. In diabetes, hyperglycemia further aggravates insulin resistance as well as beta cell dysfunction but the mechanisms causing this phenomenon, i.e. glucotoxicity, are not fully understood.. Insulin resistance can be demonstrated in healthy first-degree relatives of type 2 diabetes patients who also have a high risk of developing type 2 diabetes. Relatives and control subjects without family history of diabetes were studied with respect to insulin sensitivity and the activity in the autonomic nervous system (ANS) and in the cortisol axis. Levels of sex hormones, leptin and cytokines were analysed. Abdominal adipose tissue distribution was determined with computed tomography.. Male relatives had decreased testosterone levels and increased leptin levels. There ...
Insulin resistance is a condition in which body cells do not fully respond to the action of insulin, a hormone that controls the amount of sugar (glucose) in the blood. As a result, blood sugar levels become abnormally high.. Over time, insulin resistance can result in consistently high blood sugar levels, which increases a persons risk for type 2 diabetes. Pregnant women who are insulin resistant have an increased risk for gestational diabetes.. Usually, insulin resistance develops in people who are overweight and not physically active. These characteristics are often associated with having high cholesterol and high blood pressure. People who are insulin resistant have an increased risk of heart disease and stroke, especially if other risk factors, such as being a smoker or having high cholesterol levels, are present. ...
A progressive decline in circulating androgens was observed with advancing age. Patients 21-30 years old had lower plasma glucose and insulin levels, lower area under the oral glucose tolerance test curve and lower homeostasis model assessment of insulin resistance index, and higher glucose/insulin and quantitative insulin sensitivity check index than patients 31-39 years old. The prevalence of PCOS phenotypes changed with age. More specifically, the distribution of the phenotypes did not differ substantially between patients ≤20 years old and patients 21-30 years old. However, a decline in the prevalence of phenotype 1 (characterized by anovulation, hyperandrogenemia, and polycystic ovaries) and an increase in the prevalence of phenotype 4 (characterized by anovulation and polycystic ovaries without hyperandrogenemia) were observed in patients 31-39 years old.. Conclusion(s): ...
Insulin resistance is a common finding in hypertensive humans and animal models. The Dahl salt-sensitive (S) rat is an ideal model of genetically predetermined insulin resistance and salt-sensitive hypertension. Along the insulin signaling pathway, the insulin receptor substrates 1 and 2 (IRS-1 and -2) are important mediators of insulin signaling. IRS-1 and/or IRS-2 genetic variant(s) and/or enhanced serine phosphorylation correlate with insulin resistance. The present commentary was designed to highlight the significance of IRS-1 and/or -2 in the pathogenesis of insulin resistance. An emphasis will be given to the putative role of IRS-1 and/or -2 genetic variant(s) and serine phosphorylation in precipitating insulin resistance.. ...
NAM Publications HIV & AIDS Information :: Diabetes. Insulin resistance is seen in Syndrome X a metabolic disorder with similar symptoms to HAART-associated lipodystrophy that occurs in HIV-negative people. Syndrome X may be corrected in some cases by the restoration of insulin sensitivity, using an anti-diabetes drug called metformin.. There is now evidence that metformin may be effective in reducing insulin resistance and abdominal fat in HIV-infected people on HAART. French doctors reported that metformin reduced insulin resistance, reduced triglyceride levels and improved abdominal fat distribution in a randomised study of 25 people receiving PIs.1 HIV wasting expert, Dr Carl Grunfeld, has also reported that metformin has shown the best results in the treatment of HAART-associated insulin resistance and diabetes, producing an associated decrease in body fat.. There is also evidence from randomised, controlled studies which suggests metformin is an effective treatment for insulin resistance ...
Fingerprint Dive into the research topics of Effect of vitamin D3 supplementation on insulin resistance and β-cell function in prediabetes: a double-blind, randomized, placebo-controlled trial. Together they form a unique fingerprint. ...
What is most interesting about our recent study is that it supports the idea that increasing fat breakdown may decrease insulin resistance in muscle, said Dr. Zwetsloot. Its exciting to be part of research that gives us a better understanding of insulin resistance, and that may result in new ways to prevent and treat the condition, especially if it advocates exercise.. The jury is still out, but decades of metabolic research suggests that exercising at a moderate pace for longer periods more effectively burns fat than short, intensive exercise.. Zwetsloots studies used either exercise or an anti-diabetic medication to decrease insulin resistance. In both cases, the treatments also caused an increase in fat breakdown. The studies acknowledge that more work needs to be done to fully understand insulin resistance, but suggest that increasing fat use as an energy source (such as by exercising) may help to alleviate insulin resistance. Zwetsloot, who earned her Ph.D. in bioenergetics at East ...
Increased adiposity and unhealthy lifestyle augment the risk for type 2 diabetes in children with familial predisposition. Insulin resistance (IR) is an excellent clinical marker for identifying children at high risk for type 2 diabetes. This study was conducted to investigate parental, physiological, behavioral and socio-economic factors related to IR in Korean children. This study is a cross-sectional study using data from 111 children aged 7 years and their parents. Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated using fasting glucose and insulin level as a marker of IR. All childrens adiposity indices (r = 0.309-0.318, all P-value = 0.001) and maternal levels of fasting insulin (r = 0.285, P-value = 0.003) and HOMA-IR (r = 0.290, P-value = 0.002) were positively correlated with childrens HOMA-IR level. There was no statistical difference of childrens HOMA-IR level according to childrens lifestyle habits and socioeconomic status of families. An increase of 1 percentage
Increased adiposity and unhealthy lifestyle augment the risk for type 2 diabetes in children with familial predisposition. Insulin resistance (IR) is an excellent clinical marker for identifying children at high risk for type 2 diabetes. This study was conducted to investigate parental, physiological, behavioral and socio-economic factors related to IR in Korean children. This study is a cross-sectional study using data from 111 children aged 7 years and their parents. Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated using fasting glucose and insulin level as a marker of IR. All childrens adiposity indices (r = 0.309-0.318, all P-value = 0.001) and maternal levels of fasting insulin (r = 0.285, P-value = 0.003) and HOMA-IR (r = 0.290, P-value = 0.002) were positively correlated with childrens HOMA-IR level. There was no statistical difference of childrens HOMA-IR level according to childrens lifestyle habits and socioeconomic status of families. An increase of 1 percentage
TY - JOUR. T1 - Targeting BCAA catabolism to treat obesity-associated insulin resistance. AU - Zhou, Meiyi. AU - Shao, Jing. AU - Wu, Cheng Yang. AU - Shu, Le. AU - Dong, Weibing. AU - Liu, Yunxia. AU - Chen, Mengping. AU - Wynn, R. Max. AU - Wang, Jiqiu. AU - Wang, Ji. AU - Gui, Wen Jun. AU - Qi, Xiangbing. AU - Lusis, Aldons J.. AU - Li, Zhaoping. AU - Wang, Weiqing. AU - Ning, Guang. AU - Yang, Xia. AU - Chuang, David T.. AU - Wang, Yibin. AU - Sun, Haipeng. N1 - Funding Information: Funding. This work was supported by the Ministry of Science and Technology of China (grant nos. 2012BAI02B05 and 2013YQ030923), the National International Science Cooperation Foundation (grant no. 2015DFA30560), the National Natural Science Foundation of China (grant nos. NSFC81570717 and 81522011), the National Institutes of Health (grant nos. HL108186, HL103205, HL098954, and DK62306), the National Heart, Lung, and Blood Institute (grant no. HL080111), the Laubisch Fund (to the University of California Los ...
Type 2 diabetes is usually preceded by a long and clinically silent period of increasing insulin resistance. The purpose of this study is to demonstrate that rosiglitazone and metformin fixed-dose combination therapy (RSG/MET) will safely and effectively control glycemia as a first line of oral therapy, better than rosiglitazone (RSG) or metformin (MET) monotherapy in Korean type 2 diabetes patients. METHODS: This study was a 32-week, multicenter, randomized, double-blind study. Twenty-seven type 2 diabetes patients (males 14; females 13) were included and randomly divided into the rosiglitazone, metformin group, or rosiglitazone /metformin combination groups. The primary objective of this study was to determine the change in HbA1c from baseline (week 0) to week 32. The secondary end-points were to determine changes in fasting plasma glucose (FPG) and homeostasis model assessment insulin resistance (HOMA-IR), from baseline to week 32. Other cardiovascular risk markers were also assessed. ...
TY - JOUR. T1 - High serum resistin is associated with an increase in adiposity but not a worsening of insulin resistance in Pima Indians. AU - de Courten, Barbora. AU - Considine, Robert V. AU - Degawa-Yamauchi, Mikako. AU - Tataranni, P Antonio. PY - 2004/5/1. Y1 - 2004/5/1. N2 - Resistin is an adipokine with putative prodiabetogenic properties. Like other hormones secreted by adipose tissue, resistin is being investigated as a possible etiologic link between excessive adiposity and insulin resistance. Although there is growing evidence that circulating levels of this adipokine are proportional to the degree of adiposity, an effect on insulin resistance in humans remains unproven. To evaluate the relations among resistin, obesity, and insulin resistance, we measured fasting serum resistin levels in 113 nondiabetic (75-g oral glucose tolerance test) Pima Indians (ages 29 ± 7 years, body fat 31 ± 8%, resistin 3.7 ± 1.1 ng/ml [means ± SD]), who were characterized for body composition ...
TNF-α is an inflammatory cytokine that plays an important role in insulin resistance observed in obesity and chronic inflammation. Many cellular components involved in insulin signaling cascade are known to be inhibited by TNF-α. Insulin receptor substrate (IRS)-1 is one of the major targets in TNF-α-induced insulin resistance. The serine phosphorylation of IRS-1 enables the inhibition of insulin signaling. Until now, many studies have been conducted to investigate the mechanism of TNF-α-induced insulin resistance based on Western blot. Intracellular protein kinase crosstalk is commonly encountered in inflammation-associated insulin resistance. The crosstalk among the signaling molecules obscures the precise role of kinases in insulin resistance. We have developed a cell lysis-free quantum dots (QDots) multicolor cellular imaging to identify the biochemical role of multiple kinases (p38, JNK, IKKβ, IRS1ser, IRS1tyr, GSK3β, and FOXO1) in inflammation-associated insulin resistance pathway with a
ENGLISH ABSTRACT: Background: The aetiopathogenesis of type 2 diabetes and the associated insulin resistance have been shown to have a strong genetic basis. Several genetic variants of the peroxisome proliferatoractivated receptor gamma (PPARG) and the insulin receptor substrate (IRS) 1 genes have been associated with the metabolic states of obesity, insulin resistance and type 2 diabetes in Caucasian populations. Furthermore, insulin resistance is strongly associated with diabetes and subsequent cardiovascular disease. These are increasingly common in low- to middle -income countries, including South Africa. Limited information is currently available regarding genetic associations with insulin resistance in African populations. Objectives: (1) To identify subjects with insulin resistance and determine the frequencies of the single nucleotide polymorphisms in the PPARG and IRS1 genes and examine the associated risk of insulin resistance and type 2 diabetes mellitus in a mixed-ancestry South ...
TY - JOUR. T1 - Clinical evaluation of insulin resistance and β-cell function by the homeostasis model assessment in patients with systemic lupus erythematosus. AU - Tso, Tim K.. AU - Huang, Hui Yu. AU - Chang, Chen Kang. AU - Huang, Wen Nan. AU - Liao, Ying Ju. PY - 2004/10/1. Y1 - 2004/10/1. N2 - The aim of this preliminary study was to evaluate insulin resistance and secretion using homeostasis model assessment (HOMA) in patients with systemic lupus erythematosus (SLE). The fasting glucose and insulin concentrations, HOMA insulin resistance (IR), HOMA β-cell, antidouble-stranded DNA antibodies (anti-dsDNA), C3, C4, and SLE disease activity index (SLEDAI) were determined in a total of 58 female SLE patients. All patients were classified into subgroups according to the presence of anticardiolipin antibodies (aCL + vs. aCL-) and SLEDAI scores (SLEDAI , 3 vs. SLEDAI , 3). Results showed that SLE patients with and without aCL had significantly higher fasting insulin levels, HOMA IR, and HOMA ...
TY - JOUR. T1 - Perturbation of glucose flux in the liver by decreasing F26P2 levels causes hepatic insulin resistance and hyperglycemia. AU - Wu, Chaodong. AU - Khan, Salmaan A.. AU - Peng, Li Jen. AU - Li, Honggui. AU - Carmella, Steven G.. AU - Lange, Alex J.. N1 - Copyright: Copyright 2008 Elsevier B.V., All rights reserved.. PY - 2006. Y1 - 2006. N2 - Hepatic insulin resistance is one of the characteristics of type 2 diabetes and contributes to the development of hyperglycemia. How changes in hepatic glucose flux lead to insulin resistance is not clearly defined. We determined the effects of decreasing the levels of hepatic fructose 2,6-bisphosphate (F26P2), a key regulator of glucose metabolism, on hepatic glucose flux in the normal 129J mice. Upon adenoviral overexpression of a kinase activity-deficient 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase, the enzyme that determines F26P2 level, hepatic F26P2 levels were decreased twofold compared with those of control virus-treated mice ...
Background and aim: Acanthosis nigricans (AN) is characterized by hyperpigmented velvety plaques of body folds and neck. Insulin can have a role in the pathogenesis of this disease and hyperinsulinemia as a consequence of insulin resistance may stimulate the formation of the characteristic plaques of AN. In this study insulin resistance was compared in obese women with and without AN.Materials and Methods: Glucose tolerance test (GTT) and fasting blood insulin were measured in two groups of obese women (BMI|30 kg/m2) with AN (32 cases) and without AN (34 cases) and insulin resistance was determined using HOMA formula.Results: The mean fasting blood insulin in two groups with and without AN were 15.5±8.5 and 12.2±4.1 IU/mL; respectively (P|0.05). The mean of insulin resistance in two groups with and without AN were 3.5±1.9 and 2.6±0.9; respectively (P|0.05). The results of GTT showed that the mean fasting blood sugar was 89.5±12 mg/dl and following using glucose were 144±7 mg/dl after 30 minutes,
TY - JOUR. T1 - Proinsulin-to-C-peptide ratio versus proinsulin-to-insulin ratio in the prediction of incident diabetes. T2 - The Insulin Resistance Atherosclerosis Study (IRAS). AU - Loopstra-Masters, R. C.. AU - Haffner, S. M.. AU - Lorenzo, C.. AU - Wagenknecht, L. E.. AU - Hanley, A. J.. PY - 2011/12/1. Y1 - 2011/12/1. N2 - Aims: Associations of proinsulin-to-insulin ratios with incident type 2 diabetes have been inconsistent. The use of C-peptide as the denominator in the ratio may allow for better prediction because C-peptide concentration is not affected by hepatic insulin clearance. The objective of this paper was to compare fasting intact and split proinsulin-to-insulin ratios (PI/I, SPI/I) with intact and split proinsulin-to-C-peptide ratios (PI/C-pep, SPI/C-pep) in the prediction of type 2 diabetes. Methods: Prospective data on 818 multi-ethnic adults without diabetes at baseline from the Insulin Resistance Atherosclerosis Study (IRAS) were used. Insulin sensitivity (S I) and acute ...
TY - JOUR. T1 - 12/15-Lipoxygenase is equired for the early onset of high fat diet-induced adipose tissue inflammation and insulin resistance in mice. AU - Sears, Dorothy D.. AU - Miles, Philip D.. AU - Chapman, Justin. AU - Ofrecio, Jachelle M.. AU - Almazan, Felicidad. AU - Thapar, Divya. AU - Miller, Yury I.. PY - 2009/9/29. Y1 - 2009/9/29. N2 - Background: Recent understanding that insulin resistance is an inflammatory condition necessitates searching for genes that regulate inflammation in insulin sensitive tissues. 12/15-lipoxygenase (12/15LO) regulates the expression of proinflammatory cytokines and chemokines and is implicated in the early development of diet-induced atherosclerosis. Thus, we tested the hypothesis that 12/15LO is involved in the onset of high fat diet (HFD)-induced insulin resistance. Methodology/Principal Findings: Cells over-expressing 12/15LO secreted two potent chemokines, MCP-1 and osteopontin, implicated in the development of insulin resistance. We assessed adipose ...
TY - JOUR. T1 - Elevated Fibroblast growth factor 21 (FGF21) in obese, insulin resistant states is normalised by the synthetic retinoid Fenretinide in mice. AU - Morrice, Nicola. AU - Mcilroy, George D.. AU - Tammireddy, Seshu R.. AU - Reekie, Jennifer. AU - Shearer, Kirsty D.. AU - Doherty, Mary K.. AU - Delibegovi??, Mirela. AU - Whitfield, Phillip D.. AU - Mody, Nimesh. PY - 2017/3/3. Y1 - 2017/3/3. N2 - Fibroblast growth factor 21 (FGF21) has emerged as an important beneficial regulator of glucose and lipid homeostasis but its levels are also abnormally increased in insulin-resistant states in rodents and humans. The synthetic retinoid Fenretinide inhibits obesity and improves glucose homeostasis in mice and has pleotropic effects on cellular pathways. To identify Fenretinide target genes, we performed unbiased RNA-seq analysis in liver from mice fed high-fat diet ± Fenretinide. Strikingly, Fgf21 was the most downregulated hepatic gene. Fenretinide normalised elevated levels of FGF21 in ...
BACKGROUND: Obesity is a strong risk factor for resistance to insulin-mediated glucose disposal, a precursor of type 2 diabetes and other disorders. However, not all obese individuals are insulin resistant. We sought to identify the molecular pathways that might cause obesity-associated insulin resistance in humans by studying the morbidly obese who were insulin sensitive versus insulin resistant, thereby eliminating obesity as a variable. METHODS: Combining gene expression profiling with computational approaches, we determined the global gene expression signatures of omental and subcutaneous adipose tissue samples obtained from similarly obese patients undergoing gastric bypass surgery. RESULTS: Gene sets related to chemokine activity and chemokine receptor binding were identified as most highly expressed in the omental tissue from insulin-resistant compared with insulin-sensitive subjects, independent of the body mass index. These upregulated genes included chemokines (C-C motif) ligand 2, 3, 4, and
Approximately 50% to 70% of women with polycystic ovary syndrome (PCOS) have some degree of insulin resistance, and obesity is known to worsen insulin resistance. According to the study by the Ewha Womans University School of Medicine, posted in PubMed, ISI was significantly lower in both lean and ow/ob women with PCOS compared to BMI-matched controls (p,0.05). Increasing BMI by 1 kg/m(2) decreased ISI by 0.169 in PCOS patients (p,0.05) and by 0.238 in controls (p,0.05); there was no significant difference between these groups. In lean PCOS patients and lean controls, BMI had no effect on ISI. Multiple regression analysis revealed that PCOS status (β=-0.423, p,0.001) and BMI (β=-0.375, p,0.001) were significantly associated with ISI. Conclusion: Insulin resistance is an intrinsic defect of PCOS, and a high BMI could exacerbate insulin resistance in all women, irrespective of whether they have PCOS. ...
Blueberries are a rich source of polyphenols, which include anthocyanin bioactive compounds. Epidemiological evidence indicates that incorporating blueberries into the diet may lower the risk of developing type 2 diabetes (T2DM). These findings are supported by pre-clinical and clinical studies that have shown improvements in insulin resistance (i.e., increased insulin sensitivity) after obese and insulin-resistant rodents or humans consumed blueberries. Insulin resistance was assessed by homeostatic model assessment-estimated insulin resistance (HOMA-IR), insulin tolerance tests, and hyperinsulinemic-euglycemic clamps. Additionally, the improvements in glucose tolerance after blueberry consumption were assessed by glucose tolerance tests. However, firm conclusions regarding the anti-diabetic effect of blueberries cannot be drawn due to the small number of existing clinical studies. Although the current evidence is promising, more long-term, randomized, and placebo-controlled trials are needed to
Our cross-sectional analysis indicated a positive association between plasma aldosterone levels and insulin resistance. However, this association may be an epiphenomenon. Accordingly, we hypothesized that high levels of plasma aldosterone could predict the development of insulin resistance. Our results confirmed the hypothesis in subjects without insulin resistance at baseline. Although a recent prospective study from the Framingham Offspring Study29 has demonstrated that higher aldosterone levels are associated with the development of metabolic syndrome, they failed to demonstrate the association of aldosterone with the development of insulin resistance. The reason was not clear, but they stated in their limitations that, for the calculation of HOMA-insulin resistance, they used glucose and insulin 4 years before the baseline examination. Another explanation may be the racial difference, including the demographic backgrounds of the subjects, such as the prevalence of obesity; mean BMI in the ...
Non-alcoholic fatty liver disease (NAFLD) may result from obesity accompanied by insulin resistance and adipose tissue inflammation or from the common genetic variants in PNPLA3 (rs738409, C,G/I148M), TM6SF2 (rs58542926, C,T/E167K) and MBOAT7 (rs641738, C,T). These variants increase the liver fat content and the severity of NAFLD without features of insulin resistance. This thesis aimed to determine the following: i) whether NAFLD predicts type 2 diabetes independent of obesity and other known risk factors; ii) whether adipose tissue is inflamed in subjects homozygous for the PNPLA3 I148M variant; iii) whether obesity and insulin resistance rather than liver fat content increase coagulation factor activities and expression; and iv) which factors predict NAFLD and liver stiffness during an 11-year follow-up period. The present thesis includes one systematic review, two cross-sectional studies and one longitudinal study. Study subjects comprised Finnish adult men and women. Liver fat content was ...
Acylcarnitine accumulation in skeletal muscle and plasma has been observed in numerous models of mitochondrial lipid overload and insulin resistance. Fish oil n3PUFA (omega-3 polyunsaturated fatty acids) are thought to protect against lipid-induced insulin resistance. The present study tested the hypothesis that the addition of n3PUFA to an intravenous lipid emulsion would limit muscle acylcarnitine accumulation and reduce the inhibitory effect of lipid overload on insulin action. On three occasions, six healthy young men underwent a 6-h euglycaemic-hyperinsulinaemic clamp accompanied by intravenous infusion of saline (Control), 10% Intralipid® [n6PUFA (omega-6 polyunsaturated fatty acids)] or 10% Intralipid®+10% Omegaven® (2:1; n3PUFA). The decline in insulin-stimulated whole-body glucose infusion rate, muscle PDCa (pyruvate dehydrogenase complex activation) and glycogen storage associated with n6PUFA compared with Control was prevented with n3PUFA. Muscle acetyl-CoA accumulation was greater ...
Acylcarnitine accumulation in skeletal muscle and plasma has been observed in numerous models of mitochondrial lipid overload and insulin resistance. Fish oil n3PUFA (omega-3 polyunsaturated fatty acids) are thought to protect against lipid-induced insulin resistance. The present study tested the hypothesis that the addition of n3PUFA to an intravenous lipid emulsion would limit muscle acylcarnitine accumulation and reduce the inhibitory effect of lipid overload on insulin action. On three occasions, six healthy young men underwent a 6-h euglycaemic-hyperinsulinaemic clamp accompanied by intravenous infusion of saline (Control), 10% Intralipid® [n6PUFA (omega-6 polyunsaturated fatty acids)] or 10% Intralipid®+10% Omegaven® (2:1; n3PUFA). The decline in insulin-stimulated whole-body glucose infusion rate, muscle PDCa (pyruvate dehydrogenase complex activation) and glycogen storage associated with n6PUFA compared with Control was prevented with n3PUFA. Muscle acetyl-CoA accumulation was greater ...
Polycystic ovarian syndrome is most common endocrine disease and metabolic disorder in adolescence and reproductive women. In PCOS women insulin resistance thought to be the uniting pathogenic factor in the development of glucose intolerance, obesity, lipid abnormalities, HTN and coronary artery disease .This study is under taken to measure insulin resistance in PCOS and to see the relationship of insulin resistance with serum lipoprotein ratio. Case control study was done taking 60 women PCOS and 60 age matched healthy women as controls.In all the subjects, concentrations of fasting plasma glucose, serum TG, serum TC and HDL were estimated using enzymatic methods in semiautoanalyser. Fasting serum insulin and was measured by CLIA using Lumax-CLIA microplate reader. HOMA IR, serum LDL concentration, serum TC:HDL ratio, serum TG:HDL ratio and serum LDL:HDL ratio were calculated from estimated parameters.The mean concentrations of all the parameters were significantly increased in women with
Under fasting conditions, increases in circulating concentrations of glucagon maintain glucose homeostasis via the induction of hepatic gluconeogenesis. Triggering of the cAMP pathway in hepatocytes stimulates the gluconeogenic program via the PKA-mediated phosphorylation of CREB and dephosphorylation of the cAMP regulated CREB coactivators CRTC2 and CRTC3. In parallel, decreases in circulating insulin also increase gluconeogenic gene expression via the de-phosphorylation and activation of the forkhead transcription factor FOXO1. Hepatic gluconeogenesis is increased in insulin resistance where it contributes to the attendant hyperglycemia. Whether selective activation of the hepatic CREB/CRTC pathway is sufficient to trigger metabolic changes in other tissues is unclear, however. Modest hepatic expression of a phosphorylation-defective and therefore constitutively active CRTC2S171,275A protein increased gluconeogenic gene expression under fasting as well as feeding conditions. Circulating ...
Objective: Acromegaly is a rare pituitary disease due to excessive secretion of GH. Insulin resistance, impaired glucose tolerance (IGT) and diabetes mellitus (DM) are common features in acromegaly. Seventy-four active acromegalic patients were retrospectively evaluated in order to determine the impact of family history for diabetes mellitus on glucose tolerance, insulin resistance and beta-cell function.. Patients and methods: We studied 74 patients with active acromegaly (mean IGF-1 value: 576.8±35.6 ng/ml ES; mean GH value on OGTT nadir 11.8±1.8 ng/ml ES), 29 males and 45 females, aged 50.4±14.1 years, body mass index (BMI) 28.1±4.3 (kg/m2). All patients underwent an oral glucose tolerance test (OGTT): GH, blood glucose and insulin were sampled at 0, 30, 60, 90, 120 minutes. Insulin resistance was evaluated with HOMA2-IR, Quicki and ISI0.120; beta cell function was evaluated with HOMA2%-ß index.. Results: Acromegalic patients with a positive family history for diabetes mellitus showed an ...
Rapid, clinical improvements in type 2 diabetes occur after RYGB (4,5), yet little is known regarding the relative contribution of insulin-sensitive tissues. To determine this, we measured hepatic and muscle insulin sensitivity with a hyperinsulinemic-euglycemic clamp. Our major finding was that at 1 month after RYGB, hepatic insulin sensitivity improved whereas skeletal muscle insulin sensitivity did not. In addition, hepatic and peripheral insulin sensitivity was not influenced by surgical removal of the omentum, as postoperative values were similar in the groups who did and did not undergo omentectomy. Lima et al. (13) reported that omentectomy did not affect peripheral insulin sensitivity at 1 month after RYGB, but they did not directly assess hepatic insulin sensitivity. We have previously reported that omentectomy does not influence metabolic outcomes of RYGB after long-term follow-up (8).. The rapid and sustained improvement in diabetes after RYGB has contributed to the American Diabetes ...
Podcast: Play in new window , Download. Subscribe: Apple Podcasts , Android , RSS. In episode 99 of the Real World Wellness podcast, Christine explains the critical role that insulin plays in lowering your glucose levels and how problems occur with insulin and lead to insulin resistance before you can detect prediabetes and type 2 diabetes. Since insulin resistance is associated with metabolic syndrome, PCOS, cancer, diabetes, and many other diseases, you want to get your insulin levels tested. Christine explains the risk factors for insulin resistance and what test to ask for. She also talks about the insulin index for food and beverages and what healthy foods produce a high insulin response and should be avoided.. Resources:. https://www.ncbi.nlm.nih.gov/pubmed/18936729. https://www.ncbi.nlm.nih.gov/pubmed/17259468. https://www.ncbi.nlm.nih.gov/pubmed/18096375?log$=activity. Next Episode: Christine will talk more about strategies to increase insulin sensitivity ranging from supplements to ...
The effect of thyroid status on insulin sensitivity is of great interest but despite various studies there is conflicting data on this subject. The study group comprised of 25 female subjects each with subclinical hypothyroidism, overt hypothyroidism and euthyroid controls. Serum samples of all the patients were assayed for thyroid profile, Insulin and lipid profile. Homeostasis model of assessment (HOMA-IR) was employed to assess the level of insulin resistance. Patients with hypothyroidism demonstrated insulin resistance and dyslipidemia as observed by the higher HOMA-IR and cholesterol and triglyceride levels respectively as compared to the controls. A significantly positive correlation between TSH and HOMA-IR level was also observed in the hypothyroidism group. Thyroid dysfunction leads to alterations in glucose and lipid metabolism which is an important risk factor for cardiovascular diseases. The dyslipidemia and insulin resistance should be managed aggressively to reduce the impending risk.
Compared to healthy individuals, those with stably repressed HIV experience a higher risk of developing insulin resistance, a hallmark of pre-diabetes and a major determinant for cardiometabolic diseases. Although epigenetic processes, including in particular DNA methylation, appear to be dysregulated in individuals with insulin resistance, little is known about where these occur in the genomes of immune cells and the origins of these alterations in HIV-infected individuals. Here, we examined the genome-wide DNA methylation states of monocytes in HIV-infected individuals (n = 37) with varying levels of insulin sensitivity measured by the homeostatic model assessment of insulin resistance (HOMA-IR). By profiling DNA methylation at single-nucleotide resolution using the Illumina Infinium HumanMethylation450 BeadChip in monocytes from insulin-resistant (IR; HOMA-IR ≥ 2.0; n = 14) and insulin-sensitive (IS; HOMA-IR | 2.0; n = 23) individuals, we identified 123 CpGs with significantly different DNA
|p|Cardiovascular risk of prediabetes is still subject to controversies. We analyzed the associations between insulin resistance, adipokines and incipient atherosclerosis estimated by intima-media thickness (IMT) in a cross-sectional study on 122 prediabetic subjects without clinical signs of atherosclerotic disease. Homeostasis model assessment of insulin resistance (HOMA-IR, calculated as fasting insulin × fasting plasma glucose / 22.5), adiponectin, leptin, leptin-to-adiponectin ratio, carotid and femoral IMT were evaluated. We also assessed other parameters related to insulin resistance and adipokines (HbA1c, anthropometric and lipid parameters), as they may also influence atherosclerosis. Carotid IMT was correlated to adiponectin and leptin-to-adiponectin ratio (all p < 0.05), but not with HOMA-IR or leptin, while femoral IMT showed no relationship with these factors. After adjusting for leptin, leptin-to-adiponectin ratio, triglycerides, HDL-cholesterol, cholesterol-to-HDL ratio, triglycerides
We are interested in how skeletal muscle processes fat and its effect on insulin resistance. This is an important question since insulin resistance predates and predicts type 2 diabetes. We know that if pharmaceutical grade lipid is infused into people, they develop insulin resistance. Thus, we would like to infuse pharmaceutical grade lipid into trained subjects, believing that trained subjects will develop less insulin resistance, less decline in muscle energy function, and less accumulation of fat metabolites than untrained subjects. For comparing the effects of the pharmaceutical grade fat infusion, we will also have a group of trained and untrained subjects given a control (glycerol) infusion. Glycerol is basically the same as pharmaceutical grade lipid infusion without the lipid component.. Three visits will be required. The first visit will involve measurement of fitness. A second visit will involve measurement of insulin resistance. The third visit will involve an inpatient stay, with a ...
Author(s): Hivert, Marie-France; Cardenas, Andres; Allard, Catherine; Doyon, Myriam; Powe, Camille E; Catalano, Patrick M; Perron, Patrice; Bouchard, Luigi | Abstract: The placenta participates in maternal insulin sensitivity changes during pregnancy; however, mechanisms remain unclear. We investigated associations between maternal insulin sensitivity and placental DNA methylation markers across the genome. We analyzed data from 430 mother-offspring dyads in the Gen3G cohort. All women underwent 75-g oral glucose tolerance tests at ∼26 weeks of gestation; we used glucose and insulin measures to estimate insulin sensitivity (Matsuda index). At delivery, we collected samples from placenta (fetal side) and measured DNA methylation using Illumina EPIC arrays. Using linear regression models to quantify associations at 720,077 cytosine-guanine dinucleotides (CpGs), with adjustment for maternal age, gravidity, smoking, BMI, child sex, and gestational age at delivery, we identified 188 CpG sites where
In the present study, we have directly demonstrated that overexpression of PKC-β2 in endothelial cells inhibits insulin signaling and insulin action and increases expression of ET-1, resulting in endothelial dysfunction and accelerated atherosclerosis. These findings may help explain the elevated risk for atherosclerosis in diabetic and insulin-resistant states because PKC activation, especially the β-isoform, has been shown to be induced by hyperglycemia or elevated free fatty acids in many vascular tissues.26 The inhibiting role of PKC-β on insulin activation of eNOS clearly has been shown in endothelial cells from diabetic patients.15 At the cell signaling level, the vasotropic effects of insulin, such as the activation of eNOS, induction of heme oxygenase-1 and vascular endothelial growth factor, and downregulation of VCAM-1, are mediated through activation of the IRS/PI3K/Akt pathway.6,27,28 PKC activation, especially β-isoform, has been shown to selectively inhibit this pathway by ...
TY - JOUR. T1 - Osthol attenuates hepatic steatosis via decreased triglyceride synthesis not by insulin resistance. AU - Nam, Ho Hyun. AU - Jung, Dae Won. AU - Jeon, Hye Joon. AU - Lee, Jai Sun. AU - Saeed, Waqar Khalid. AU - Kim, Eun Kyung. PY - 2014/9/7. Y1 - 2014/9/7. N2 - AIM: To evaluate the effects of osthol on intrahepatic fat synthesis, β-oxidation, inflammation, and insulin resistance by multifaceted analysis. METHODS: Sprague-Dawley rats (n = 30) were randomly divided into control, non-alcoholic fatty liver disease (NAFLD), and osthol groups. NAFLD and osthol groups were fed with a high-fat diet for 14 wk. After 8 wk of the high-fat diet, the osthol group also received osthol 20 mg/kg orally 5 times/wk. To assess the insulin resistance, oral glucose tolerance was performed at the end of 14 wk. Immunohistochemical (4-HNE, F4/80) and hematoxylin and eosin (HE) staining were performed on liver tissue extracts after animal sacrifice at 14 wk. SREBP1c, FAS, SCD-1, PPAR-α, CROT, MCP-1, ...
What is Insulin Resistance?. Under normal circumstances, insulin is tightly controlled by a natural homoeostatic feedback mechanism. With every meal, insulin is released as carbohydrates enter the blood stream. In a healthy body, the insulin receptors in the cell membranes respond to the hormone, and take up carbohydrates and other nutrients. This, in turn, reduces the production of insulin.. The problem starts when the tissue fails to respond to insulin. When this happens, the sugar in the blood remains high despite the presence of insulin, and the body has no choice but to release more insulin. It becomes a vicious cycle because it is actually the presence of insulin that makes the tissue more and more resistant to it.. This is how insulin exposure determines the rate of ageing: with every insulin release, cell membranes become a little bit more insulin resistant. A gradual increase in insulin concentration over time is normal, but the current epidemic of severe insulin resistance is a modern ...
TY - JOUR. T1 - Insulin sensitivity and regional fat gain in response to overfeeding. AU - Votruba, Susanne B.. AU - Jensen, Michael D.. PY - 2011/2. Y1 - 2011/2. N2 - Although insulin resistance and type 2 diabetes (T2DM) are associated with upper body fat distribution, it is unknown whether insulin resistance predisposes to upper body fat gain or whether upper body fat gain causes insulin resistance. Our objective was to determine whether insulin sensitivity predicts abdominal (subcutaneous and/or visceral) fat gain in normal weight adults. Twenty-eight (15 men) lean (BMI = 22.1 2.5kg/m2), healthy adults underwent ∼8 weeks of overfeeding to gain ∼4kg fat. Body composition was assessed before and after overfeeding, using dual-energy X-ray absorptiometry (DXA) and abdominal computed tomography to measure total and regional (visceral, abdominal, and lower body subcutaneous) fat gain. We assessed insulin sensitivity with an intravenous glucose tolerance test (IVGTT) and the 24-h insulin area ...
TY - JOUR. T1 - Low-grade inflammation and muscular fitness on insulin resistance in adolescents. T2 - Results from LabMed Physical Activity Study. AU - Agostinis-Sobrinho, César A.. AU - Ramírez-Vélez, Robinson. AU - García-Hermoso, Antonio. AU - Moreira, Carla. AU - Lopes, Luís. AU - Oliveira-Santos, José. AU - Abreu, Sandra. AU - Mota, Jorge. AU - Santos, Rute. PY - 2018/5/1. Y1 - 2018/5/1. N2 - Background: Low muscular fitness (MF) and low-grade inflammation has been linked to insulin resistance (IR). Objective: To evaluate the associations between MF and a clustered score of inflammatory biomarkers on IR and to investigate the combined impact of MF and inflammation on IR in adolescents. Methods: This is a cross-sectional analysis with 529 adolescents (267 girls) aged 12 to 18 years. Pubertal stage, socioeconomic status, adherence to the Mediterranean diet, cardiorespiratory fitness, and waist circumference were assessed. Standing long-jump and isometric handgrip dynamometry were used ...
Insulin resistance occurs in around 50% to 80% of women with PCOS [12], primarily in the more severe NIH diagnosed PCOS and in those who are overweight. Lean women [13] and milder Rotterdam diagnosed PCOS [14] appear to have less severe insulin resistance. A full discussion of the complex mechanisms involved in insulin resistance, hyperinsulinaemia, DM2 and CVD is beyond the scope of this review. Mechanisms involved in insulin resistance are likely to be complex with genetic and environmental contributors. Specific abnormalities of insulin metabolism identified in PCOS include reductions in secretion [39, 40], reduced hepatic extraction [40], impaired suppression of hepatic gluconeogenesis [41] and abnormalities in insulin receptor signalling [42]. Interestingly, there is a paradoxical expression of insulin resistance in PCOS whereby insulin-stimulated androgen production persists while its role in glucose metabolism is impaired [42]. Therefore, insulin resistance in PCOS results in ...
Polycystic ovary syndrome (PCOS) is associated with an increased risk of insulin resistance (IR), metabolic syndrome (MetS), impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM). Metabolic aspects of the four PCOS phenotypes remain to be fully defined. The aim of this study was to compare metabolic parameters and insulin resistance among the four PCOS phenotypes defined according to the Rotterdam criteria and to determine predictors of these complications. A total of 526 reproductive-aged women were included in this observational case-control study. Of these, 263 were diagnosed as a PCOS based on Rotterdam criteria and 263 infertile women with no evidence of PCOS were recruited as controls. Biochemical, metabolic and insulin resistance parameters were compared in the two groups and the frequency of MetS and IR were compared among the four phenotypes. Data were analyzed for statistical significance using Students t-test and one way analysis of variance followed by a post-hoc test (least
TY - JOUR. T1 - Dietary phosphate modulates atherogenesis and insulin resistance in apolipoprotein E knockout mice--brief report. AU - Ellam, Timothy. AU - Wilkie, Martin. AU - Chamberlain, Janet. AU - Crossman, David. AU - Eastell, Richard. AU - Francis, Sheila. AU - Chico, Timothy J A. PY - 2011/9. Y1 - 2011/9. N2 - Epidemiological studies link higher serum phosphate and the phosphatonin fibroblast growth factor 23 with cardiovascular events and atheroma, and they link lower serum phosphate with insulin resistance and the metabolic syndrome. We investigated whether manipulating dietary phosphate influences atherogenesis or insulin sensitivity in mice.. AB - Epidemiological studies link higher serum phosphate and the phosphatonin fibroblast growth factor 23 with cardiovascular events and atheroma, and they link lower serum phosphate with insulin resistance and the metabolic syndrome. We investigated whether manipulating dietary phosphate influences atherogenesis or insulin sensitivity in ...
Body mass index, fasting insulin, and aspartate aminotransferase or alanine aminotransferase ratio also differed.. The team found that quantitative insulin sensitivity check index, and hyaluronic acid differed between the 2 groups.. Hyaluronic acid composite index for distinguishing steatosis from nonalcoholic steatohepatitis was calculated.. The team calculated this index by summing up risk factors that included age 50 years or more, and female gender.. Other risk factors assessed were aspartate aminotransferase 45 IU/l or more, and body mass index 30 mg/kg2 or more.. The index was also calculated by an aspartate aminotransferase/alanine aminotransferase ratio of 0.8 or more, and hyaluronic acid of 55 mcg/l or more.. The team determined the accuracy of the index by receiver operating characteristic analysis, and found this to be 0.76.. The presence of 3 or more risk factors had a sensitivity of 74% and a specificity of 66%.. In addition, the researchers noted that a hyaluronic acid cutoff of 45 ...
An overweight child, or a child with a tendency to carry excess weight around the waist - may be at risk of being INSULIN RESISTANT!. In South Africa, about one in three children are overweight!. 80 % of individuals that are overweight are insulin resistant.. Children with Insulin Resistance have a very good chance of getting diabetes within 2 years of being diagnosed with insulin resistance if it is not treated successfully.. Insulin Resistance in children (as with adults) is also associated with an increased incidence (the chance of getting something) of heart disease, stroke or being overweight later in life.. When is a child at risk of developing or having Insulin Resistance?. -Any child or teenager who is overweight especially if they carry excess weight around their stomach, is at risk of developing or having insulin resistance ...
Why are Asian Americans at higher risk of developing type 2 diabetes than Caucasian Americans, and prone to develop the disease at lower body weights? One part of this puzzle may lie in the transition from traditional high-fiber, low-fat Asian diets to current westernized diets, which may pose extra risks for those of Asian heritage, says George King, M.D., Senior Vice President and Chief Scientific Officer at Joslin Diabetes Center and the senior author of the study.. A Joslin randomized clinical trial now has demonstrated that both Asian Americans and Caucasian Americans at risk of type 2 diabetes who adopted a rigorously controlled traditional Asian diet lowered their insulin resistance. (A leading risk factor for developing the disease, insulin resistance is a condition in which the body struggles to use the hormone insulin, which helps to metabolize sugar.). Moreover, when both groups of participants then switched to consuming typical western fare, the Asian Americans experienced greater ...
For one, it can make it very difficult for you to control your weight. More importantly, this is a prediabetic state that puts you at a much higher risk for developing diabetes and having a heart attack. Often people with insulin resistance struggle to maintain their weight, even though they may only eat one meal a day.. It is not always how much you eat, but what you eat.. People with insulin resistance develop higher than normal levels of insulin in their blood. Insulin is a hormone produced by the pancreas that helps to keep our blood sugar normal. People with insulin resistance do not metabolize carbohydrates (sugar, pasta, potatoes, etc) the same as those without. As they continue to eat a diet high in carbohydrates, their cells dont want to take in any more sugar or fat, so they become RESISTANT. The pancreas then has to produce more insulin to control the blood sugar. The insulin rapidly moves the blood sugar into fat, muscle and liver cells. Sugar in fats cells gets turned fat ...
All previous studies that investigated the association between abdominal fat distribution and insulin resistance evaluated subcutaneous and visceral fat area and/or volume, but these values were not related to the body type of each subject. In the present study we have examined the association between abdominal fat distribution and peripheral (muscle)/hepatic sensitivity to insulin using the visceral to abdominal subcutaneous fat area ratio (VF/SF ratio) in male patients with type 2 diabetes mellitus. This ratio defines the predominancy of visceral or subcutaneous abdominal adiposity, independent of the body type of each individual. Thirty-six type 2 diabetic male patients underwent a euglycemic insulin clamp (insulin infusion rate = 40 mU/m2·min) with 3-3H-glucose to measure insulin-mediated total body (primarily reflects muscle) glucose disposal (TGD) and suppression of endogenous (primarily reflects liver) glucose production (EGP) in response to a physiologic increase in plasma insulin concentration
During recent times we are dealing with multiple medical complications occurring in a single pregnant woman. It is well known fact that insulin resistance is present during normal pregnancy and it is relatively diabetogenic state. In women with genetic predisposition, diabetes, hypertension and hypothyroidism complicate pregnancy resulting in increased maternal and perinatal morbidity and mortality. There was evidence in the literature regarding insulin resistance and gestational diabetes. This review analysed the literature regarding the association of diabetes, hypertension and hypothyroidism and found that there is a linkage between these three disorders in pregnant state and the insulin resistance develops by multiple molecular mechanisms both centrally and in peripheral tissues. The key mechanism is insulin receptor substrate-1 (IRS-1) which gets inactivated by serine phosphorylation and leads to hyperglycaemia which in turn leads to stimulation of beta cells of pancreas and leads to ...
We also evaluated if vimentin affects insulin resistance in HFD-fed obese mice and found that Vim−/− mice had significantly lower fasting glucose level and improved glucose tolerance compared to control mice. In contrast, there was no difference in blood insulin level between the two groups (Fig. 2D). GLUT4, the predominant insulin-responsive glucose transporter isoform, plays a key role in the transport of extracellular glucose into insulin-sensitive cells in vivo [29,30,31]. There have been several studies revealing the role of GLUT4 in diabetes in mice. Overexpression of GLUT4 in fat reversed insulin resistance in muscle-GLUT4−/− mice [32]. GLUT4 overexpression improved insulin sensitivity and fasting triglyceridemia in HFD-fed transgenic mice [33]. In our study, GLUT4 was 22% lower in total cell lysates and 50.3% lower in the membrane fraction of vimentin-null adipocytes (Fig. 3E). Our finding corresponds to a previous report that vimentin mediates insulin-sensitive GLUT4 ...
Abstract: Obesity is a major risk factor for insulin resistance (IR) and its attendant complications. The pathogenic mechanisms linking them remain poorly understood, partly due to a lack of intermediary monogenic human phenotypes. Here, we report on a monogenic form of IR-prone obesity, Alström syndrome (ALMS). Twenty-three subjects with monogenic or polygenic obesity underwent hyperinsulinaemic-euglycemic clamping with concomitant adipose tissue (AT) microdialysis and an in-depth analysis of subcutaneous AT histology. We have shown a relative adipose tissue failure in monogenic obese cohort; a finding supported by observations in a novel conditional mouse model (Almsflin/flin) and ALMS1-silenced human primary adipocytes. Whereas, selective reactivation of ALMS1 gene in adipose tissue of an ALMS conditional knockdown mice model (Almsflin/flin;Adipo-Cre+/-) restores systemic insulin sensitivity and glucose tolerance. Hence, we show for the first time the relative adipose tissue failure in human ...
Insulin resistance[edit]. Activation of PKC-θ by diacylglycerol may cause insulin resistance in muscle by decreasing IRS1- ... "Insulin receptor Thr1160 phosphorylation mediates lipid-induced hepatic insulin resistance". Journal of Clinical Investigation ... "Diacylglycerol-mediated insulin resistance". Nature Medicine. 16 (4): 400-402. doi:10.1038/nm0410-400. PMC 3730126. PMID ... associated PI3K activity.[8] Similarly, activation of PKCε by diacyglycerol may cause insulin resistance in the liver.[8][9] ...
insulin receptor (Rabson-Mendenhall syndrome). *Insulin resistance. Hyperfunction. *Hypoglycemia. *beta cell (Hyperinsulinism) ...
insulin receptor (Rabson-Mendenhall syndrome). *Insulin resistance. Hyperfunction. *Hypoglycemia. *beta cell (Hyperinsulinism) ... Glycemic control is maintained mainly with insulin in patients with Type 1 DM and with hypoglycemic agents and/or insulin in ... some patients with insulin-dependent DM may find that their regular insulin doses are lasting longer than normal, or that they ... About half of insulin is metabolized and cleared by the kidneys. This means that as kidney function worsens in the setting of ...
insulin receptor (Rabson-Mendenhall syndrome). *Insulin resistance. Hyperfunction. *Hypoglycemia. *beta cell (Hyperinsulinism) ...
insulin receptor (Rabson-Mendenhall syndrome). *Insulin resistance. Hyperfunction. *Hypoglycemia. *beta cell (Hyperinsulinism) ...
insulin receptor (Rabson-Mendenhall syndrome). *Insulin resistance. Hyperfunction. *Hypoglycemia. *beta cell (Hyperinsulinism) ...
insulin receptor (Rabson-Mendenhall syndrome). *Insulin resistance. Hyperfunction. *Hypoglycemia. *beta cell (Hyperinsulinism) ... Thyroid hormone resistance. Calcium homeostasis disorders and Metabolic bone disease[edit]. *Parathyroid gland disorders * ...
insulin receptor (Rabson-Mendenhall syndrome). *Insulin resistance. Hyperfunction. *Hypoglycemia. *beta cell (Hyperinsulinism) ... Enhanced glucose control methods include more frequent subcutaneous insulin administration, continuous insulin infusion, oral ... Transcutaneous electrical nerve stimulation (TENS) and interferential current (IFC) use a painless electric current and the ... and many of these more aggressive methods require more frequent insulin use which has been associated with excessive risk of ...
insulin receptor (Rabson-Mendenhall syndrome). *Insulin resistance. Hyperfunction. *Hypoglycemia. *beta cell (Hyperinsulinism) ...
Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance.[13] Insulin ... some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance ... Diabetes mellitus type 2 is characterized by high blood glucose in the context of insulin resistance and relative insulin ... insulin resistance, and relative lack of insulin.[6] Common symptoms include increased thirst, frequent urination, and ...
insulin receptor (Rabson-Mendenhall syndrome). *Insulin resistance. Hyperfunction. *Hypoglycemia. *beta cell (Hyperinsulinism) ...
... does it explain insulin resistance of puberty?". J. Clin. Endocrinol. Metab. 86 (10): 4881-6. doi:10.1210/jc.86.10.4881. PMID ...
insulin receptor (Rabson-Mendenhall syndrome). *Insulin resistance. Hyperfunction. *Hypoglycemia. *beta cell (Hyperinsulinism) ...
Insulin resistance and hypertriglyceridemia occur. Calf muscular hypertrophy may occur. Type 5 is due to mutations in the AKT2 ... Complications include hypertension, insulin resistance and hypertriglyceridemia. The gene causing this condition is not yet ... Insulin resistance is common. Other conditions associated with this condition include acanthosis nigricans, fatty liver, ... The patients also suffered from hypertension, insulin resistance and hypertriglyceridemia. Type 6 due to mutations in the CIDEC ...
Ten, Svetlana; MacLaren, Noel (2004). "Insulin resistance syndrome in children". J. Clin. Endocrinol. Metab. 89 (6): 2526-39. ... and insulin resistance.[45] A 2004 study recommended that the consumption of sucrose-containing drinks should be limited due to ... which induced visceral fat and ultimately resulted in insulin resistance.[44] Another study found that rats fed sucrose-rich ... the growing number of people with obesity and insulin resistance.[46] Human health[edit]. Human beings have long sought sugars ...
It also induces insulin resistance by promoting serine-phosphorylation of insulin receptor substrate-1 (IRS-1), which impairs ... On other tissues: increasing insulin resistance. TNF phosphorylates insulin receptor serine residues, blocking signal ... regulation of insulin secretion. • regulation of immunoglobulin secretion. • osteoclast differentiation. • regulation of tumor ... insulin signaling. *It is a potent chemoattractant for neutrophils, and promotes the expression of adhesion molecules on ...
Insulin resistance is a major feature of Diabetes Mellitus Type 2 (T2DM), and central obesity is correlated with both insulin ... For example, fat next to the liver drains into it, causing a fatty liver, which is a risk factor for insulin resistance, ... Central obesity is associated with a statistically higher risk of heart disease, hypertension, insulin resistance, and Diabetes ... Westphal, S. A. (2008). "Obesity, Abdominal Obesity, and Insulin Resistance". Clinical Cornerstone. 9 (1): 23-29; discussion 30 ...
Leptin can also be used to reverse insulin resistance and hepatic steatosis, to cause reduced food intake, and decrease blood ... May 2002). "Leptin reverses insulin resistance and hepatic steatosis in patients with severe lipodystrophy". Journal of ... Congenital generalized lipodystrophy (CGL) is a rare autosomal recessive disorder which manifests with insulin resistance, ... insulin resistance; and high serum levels of triglycerides. Genetic testing can also confirm the disease, as mutations in the ...
Role of insulin resistance in human disease. 1988". Nutrition. 13 (1): 65; discussion 64, 66. doi:10.1016/0899-9007(97)90878-9 ... Reaven's work on insulin resistance and diabetes mellitus with John W. Farquhar goes back at least to 1965.[3] ... Demonstration of the Central Role of Insulin Resistance in Type 2 Diabetes and Cardiovascular Disease". Diabetes Care. 37 (5): ... have a common cause in insulin resistance and impaired glucose tolerance.[4] Initially titled "syndrome X", the constellation ...
... as a marker of obesity-related insulin resistance". Int J Obes (Lond). 36 (11): 1442-9. doi:10.1038/ijo.2011.256. PMID 22184060 ... "Metabolic endotoxemia initiates obesity and insulin resistance". Diabetes. 56 (7): 1761-72. doi:10.2337/db06-1491. PMID ... Other studies have shown that purified endotoxin from Escherichia coli can induce obesity and insulin-resistance when injected ... recent study has uncovered a potentially contributing role for Enterobacter cloacae B29 toward obesity and insulin resistance ...
Inflammation and insulin resistance. J. Clin. Invest. 2006-07, 116 (7): 1793-801 [2016-01-03]. PMC 1483173. PMID 16823477. doi: ... Chiolero A, Faeh D, Paccaud F, Cornuz J. Consequences of smoking for body weight, body fat distribution, and insulin resistance ... Shoelson SE, Herrero L, Naaz A. Obesity, inflammation, and insulin resistance. Gastroenterology. 2007-05, 132 (6): 2169-80. ...
Shoelson SE, Lee J, Goldfine AB (2006). «Inflammation and insulin resistance». J. Clin. Invest. 116 (7): 1793-801. PMC 1483173 ... 2004). «Effect of liposuction on insulin resistance and vascular inflammatory markers in obese women». Br J Plast Surg. 57 (3 ... Shoelson SE, Herrero L, Naaz A (2007). «Obesity, inflammation, and insulin resistance». Gastroenterology. 132 (6): 2169-80. ... and insulin resistance». Am. J. Clin. Nutr. 87 (4): 801-9. PMID 18400700.. CS1-vedlikehold: Flere navn: forfatterliste (link) ...
"The endothelium abridges insulin resistance to premature aging". Journal of the American Heart Association. 2 (3): e000262. doi ... insulin-like growth factor receptor binding. • transmembrane receptor protein tyrosine kinase adaptor activity. • insulin ... Sasaoka T, Kobayashi M (Aug 2000). "The functional significance of Shc in insulin signaling as a substrate of the insulin ... insulin receptor signaling pathway. • intracellular signal transduction. • epidermal growth factor receptor signaling pathway. ...
Not enough insulin in the setting of insulin resistance[2]. Risk factors. Overweight, previously having gestational diabetes, ... More insulin is needed to overcome this resistance; about 1.5-2.5 times more insulin is produced than in a normal pregnancy.[19 ... Pregnancy causes increased insulin resistance and so a higher insulin demand. The β-cells must compensate for this by either ... Gestational diabetes is caused by not enough insulin in the setting of insulin resistance.[2] Risk factors include being ...
"Insulin Resistance in Patients with Chronic Kidney Disease". Journal of Biomedicine and Biotechnology. 2012: 1-5. doi:10.1155/ ...
Insulin resistance. *Increase protein-muscle catabolism. *Anemia due to erythropoietin deficiency and shortened red-cell ...
... is associated with an increased risk of insulin resistance. Insulin resistance refers to cell's reduced sensitivity to insulin ... Wilcox G (May 2005). "Insulin and insulin resistance". The Clinical Biochemist. Reviews. 26 (2): 19-39. PMC 1204764. PMID ... insulin resistance). Increased insulin in the blood stimulates the ovaries to produce more androgens increasing the risk of ... As demonstrated in mice, insulin resistance is a factor in poor fertility as it has an effect on oocyte development. This in ...
Wilcox, Gisela (2016-11-20). "Insulin and Insulin Resistance". Clinical Biochemist Reviews. 26 (2): 19-39. ISSN 0159-8090. PMC ... This is the more common process of insulin resistance, which leads to adult-onset diabetes. Another example can be seen in ... Elevated levels of the hormone insulin in the blood trigger downregulation of the associated receptors. When insulin binds to ... This process is illustrated by the insulin receptor sites on target cells, e.g. liver cells, in a person with type 2 diabetes. ...
Wilcox, Gisela (May 2005). "Insulin and Insulin Resistance". Clinical Biochemist Reviews. 26 (2): 19-39. ISSN 0159-8090. PMC ... Insulin normally binds to insulin receptors but in excess amounts may bind to insulin-like growth factor (IGF) receptors in ... Diabetes is associated with risk factors for various cardiovascular diseases including obesity, insulin resistance, high blood ... Insulin insensitivity in the case of type II diabetes can cause prolonged increases in blood insulin. ...
... is due to insufficient insulin production from beta cells in the setting of insulin resistance.[13] Insulin ... some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance ... In the early stages of insulin resistance, the mass of beta cells expands, increasing the output of insulin to compensate for ... Type 2 diabetes is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency.[60 ...
Major insulin resistance syndromes: clinical and physiopathological aspects]. J. Soc. Biol. 2002, 195 (3): 249-57. PMID ...
... risk indicator for increased body mass index and insulin resistance". Acta Dermato-Venereologica (Review). 93 (6): 644-9. doi: ... High levels of growth hormone (GH) and insulin-like growth factor 1 (IGF-1) are also associated with worsened acne.[42] Both ... Andriessen A, Lynde CW (November 2014). "Antibiotic resistance: shifting the paradigm in topical acne treatment". Journal of ... Both regimens are effective, but benzoyl peroxide does not lead to antibiotic resistance.[10] ...
This genetic trait confers resistance to HIV infection by blocking attachment of HIV to the cell. Roughly one in 1000 people of ... 2009). "C-peptide levels and insulin independence following autologous nonmyeloablative hematopoietic stem cell transplantation ... insulin dependent) diabetes in children and adults. Results have been promising; however, as of 2009[update] it was premature ... "The Geographic Spread of the CCR5 Δ32 HIV-Resistance Allele". PLoS Biology. 3 (11): e339. doi:10.1371/journal.pbio.0030339 ...
... and Protein Oxidation and Insulin Resistance". J. Clin. Invest. 81 (4): 1137-45. doi:10.1172/JCI113428. PMC 329642. PMID ... alcohol is also known to potentiate the insulin response of the human body to glucose, which, in essence, "instructs" the body ... "Potentiation of the Plasma Insulin Response to Glucose by Prior Administration of Alcohol" (PDF). Diabetes. 18 (8): 517-22. ...
In insulin dependent diabetes mellitus[edit]. In type 1 diabetes both DR3 and DQ2 appear to play a role. DR3-DQ2.5 can be ... Resistance to recombination[edit]. A1::DQ2 is found in Iceland, Pomors of Northern Russia, the Serbians of Northern Slavic ... therefore diet alone cannot explain its resistance to recombination. ...
It described intake of EPO, growth hormones, testosterone and insulin on 114 days during the 200-day season of 2003.[53] ... The cells would be re-injected shortly before competition, boosting resistance to fatigue. If haematocrit levels (volume of red ...
Nafiye Y, Sevtap K, Muammer D, Emre O, Senol K, Leyla M. The effect of serum and intrafollicular insulin resistance parameters ... Fasting insulin level or GTT with insulin levels (also called IGTT). Elevated insulin levels have been helpful to predict ... Insulin Resistance and the Polycystic Ovary Syndrome Revisited: An Update on Mechanisms and Implications. Endocrine Reviews. ... Reactive oxygen species-induced oxidative stress in the development of insulin resistance and hyperandrogenism in polycystic ...
Melnik BC, John SM, Plewig G (noiembrie 2013). „Acne: risk indicator for increased body mass index and insulin resistance". ...
Eccentric exercise or resistance training is currently being used as a form of rehabilitation for sport injuries, but also as ... Several recent studies have indicated that eccentric exercise as in walking down hill has greater beneficial effects on insulin ... Because the internal resistance of the device was low, the same force was being applied by both individuals, yet the task was ... Results concluded that resistance training (eccentric contractions) promoted strength gain. An increase in cardiac vagal ...
2004) Systemic inflammation-associated glucocorticoid resistance and outcome of ARDS. Ann N Y Acad Sci. 1024:24-53. Morrison RJ ... These include β2-agonists, dopamine, insulin, allopurinol, and non-steroidal anti-inflammatory drugs (NSAIDs), such as ... such as insulin, dopamine, and allopurinol have also been effective in reducing pulmonary edema in animal models but require ...
"Alzheimer's beta-amyloid peptides compete for insulin binding to the insulin receptor" (PDF). J. Neurosci. 22 (10): RC221. PMID ... "NMR solution structure of rat Aβ(1-16): toward understanding the mechanism of rats' resistance to Alzheimer's disease" ...
Niobium alloys are also used in rocket nozzles because of niobium's high corrosion resistance.[4] ... primarily for increasing insulin sensitivity[10] and body-building. Vanadyl sulfate may improve glucose control in people with ...
Beneficial effects on blood lipids and insulin resistance are due to the weight loss, not to the change in caloric composition ... Carbohydrate-insulin hypothesis[edit]. Low-carbohydrate diet advocates including Gary Taubes and David Ludwig have proposed a " ... "carbohydrate-insulin hypothesis" in which carbohydrates are said to be uniquely fattening because they raise insulin levels and ... Hall KD (2017). "A review of the carbohydrate-insulin model of obesity". Eur J Clin Nutr (Review). 71 (3): 323-326. doi:10.1038 ...
"Effects of stevioside on glucose transport activity in insulin-sensitive and insulin-resistant rat skeletal muscle". Metab. ... "Interpretation of results with the [[8-azaguanine]] resistance system in Salmonella typhimurium: no evidence for direct acting ... "Rebaudioside A potently stimulates insulin secretion from isolated mouse islets: studies on the dose-, glucose-, and calcium- ...
Antibiotic resistance tests: bacteria in the culture on the left are sensitive to the antibiotics contained in the white, paper ... Some of these include synthetic insulin which was produced in 1979 using recombinant DNA and the first genetically engineered ... Antimicrobial resistance is an increasingly problematic issue that leads to millions of deaths every year.[32] ... Stewart PS; Costerton JW (July 2001). "Antibiotic resistance of bacteria in biofilms". Lancet. 358 (9276): 135-8. doi:10.1016/ ...
Resistance to puromycin is conferred by the pac gene encoding a puromycin N-acetyl-transferase (PAC) that was found in a ... Insulin. *Agonists: Chaetochromin (4548-G05). *Insulin-like growth factor 1. *Insulin-like growth factor 2 ... Puromycin resistance in yeast can also be conferred through expression of the puromycin N-acetyl-transferase (pac) gene.[8] ... "Puromycin- and methotrexate-resistance cassettes and optimized Cre-recombinase expression plasmids for use in yeast". Yeast ...
Body weight and body fat are increased.[14] There are signs of insulin resistance, as in PCOS in humans.[14] ... GPER knockout mice have also been generated, and exhibit obesity, cardiovascular dysfunction, insulin resistance, glucose ... Estrogen insensitivity syndrome (EIS), or estrogen resistance, is a form of congenital estrogen deficiency or hypoestrogenism[2 ... Smith EP, Boyd J, Frank GR, Takahashi H, Cohen RM, Specker B, Williams TC, Lubahn DB, Korach KS (1994). "Estrogen resistance ...
2002). "Tetradecylthioacetic acid prevents high fat diet induced adiposity and insulin resistance". Journal of Lipid Research. ... and preventing high fat diet induced adiposity and insulin resistance.[3] In human clinical study, there have been mixed ...
Calbet, JA (2002). "Plasma glucagon and insulin responses depend on the rate of appearance of amino acids after ingestion of ... effects on mixed muscle protein synthesis at rest and following resistance exercise in young men". Journal of Applied ... and Insulin Responses in Human Subjects". J. Agric. Food Chem. 58 (15): 8788-8797. ...
It was developed based on the structure of the Abl-imatinib complex to address imatinib intolerance and resistance.[22][19][20] ... Insulin-like growth factor-1 (somatomedin C). *IGF-1 LR3. *Insulin-like growth factor-2 (somatomedin A) ...
Shoelson SE; Herrero L; Naaz A (maj 2007). "Obesity, inflammation, and insulin resistance". Gastroenterology. Vol. 132 no. 6. ... "Inflammation and insulin resistance". J. Clin. Invest. Vol. 116 no. 7. str. 1793-801. doi:10.1172/JCI29069. PMC 1483173. PMID ... and insulin resistance". Am. J. Clin. Nutr. Vol. 87 no. 4. str. 801-9. PMID 18400700.. CS1 vzdrževanje: Uporaba authors ... To so med drugim insulin, sulfonilsečnine, tiazolidindioni, atipični antipsihotiki, antidepresivi, glukokortikoidi, določeni ...
2007). "Insulin resistance and inflammation as precursors of frailty: the Cardiovascular Health Study". Arch Intern Med. 167 (7 ... insulin resistance,[25] glucose levels,[26] compromised altered immune function,[27][28] micronutrient deficiencies and ...
High levels of prolactin during pregnancy and breastfeeding also increase insulin resistance, increase growth factor levels ( ... The electrical impulse then ascends the posterolateral tract for one or two vertebral levels and synapses with second-order ... Following the electrical impulse, oxytocin is released into the bloodstream. Through the bloodstream, oxytocin makes its way to ... The electrical impulse follows the spinothalamic tract, which begins by innervation of fourth intercostal nerves. ...
... insulin resistance and dyslipidaemia". Diabetes, obesity & metabolism. 7 (4): 406-13. PMID 15955127. doi:10.1111/j.1463- ... Movement against gravity, but not against added resistance. Grade 4. Movement against external resistance, but less than normal ... In skeletal muscle, contraction is stimulated by electrical impulses transmitted by the nerves, the motoneurons (motor nerves) ... measuring electrical activity in muscles). In some cases, muscle biopsy may be done to identify a myopathy, as well as genetic ...
... has opposite action to ghrelin on food intake and plays a role in energy balance.[8] Circuit-resistance exercise ... "Altered distribution of adiponectin isoforms in children with Prader-Willi syndrome (PWS): association with insulin ... Ghanbari-Niaki A, Saghebjoo M, Rahbarizadeh F (2008). "single circuit-resistance exercise has no effect on plasma obestatin ...
A fall in blood glucose, causes insulin secretion to be stopped, and glucagon to be secreted from the alpha cells into the ... Homeostasis is brought about by a natural resistance to change in the optimal conditions,[2] and equilibrium is maintained by ... The arterioles are the main resistance vessels in the arterial tree, and small changes in diameter cause large changes in the ... Predictive homeostasis is an anticipatory response to an expected challenge in the future, such as the stimulation of insulin ...
Serum insulin level, homeostasis model assessment insulin resistance scores, leptin, and adiponectin levels decreased in the ... We hypothesized that the lemon detox program would reduce body weight, body fat mass, thus lowering insulin resistance and ... Lemon detox diet reduced body fat, insulin resistance, and serum hs-CRP level without hematological changes in overweight ... Therefore, we suppose that the lemon detox program reduces body fat and insulin resistance through caloric restriction and ...
Fasting insulin levels[edit]. A fasting serum insulin level greater than 25 mU/L or 174 pmol/L indicates insulin resistance. ... Modified insulin suppression test[edit]. Another measure of insulin resistance is the modified insulin suppression test ... Insulin resistance is considered a component of the metabolic syndrome. There are multiple ways to measure insulin resistance ... This link seems to exist under diverse causes of insulin resistance. It also is based on the finding that insulin resistance ...
... the body doesnt let insulin do its job as well and its harder for glucose to get into the cells. This is called insulin ... Even though the pancreas is still making insulin, ... This is called insulin resistance. People who have insulin ... but the insulin cant work the way it should. Even though the pancreas is still making insulin, the body doesnt let insulin do ... Kids who are starting to get type 2 diabetes are still able to make insulin, ...
... insulin resistance, and type 2 diabetes connection and how to reverse insulin resistance. ... How to Reverse Insulin Resistance. If you have insulin resistance, you want to become the opposite-more insulin sensitive ( ... What Causes Insulin Resistance?. It isnt clear exactly what causes insulin resistance, but a family history of type 2 diabetes ... You do not have to be overweight to have insulin resistance. You cant tell if someone has insulin resistance by looking at ...
Hyperinsulinemic-euglycemic glucose clamp Fasting insulin Homeostasis model assessment (HOMA) Quantitati... more ... There are multiple methods available to assess insulin resistance, including the following: ... encoded search term (How is insulin resistance assessed?) and How is insulin resistance assessed? What to Read Next on Medscape ... Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations ...
Insulin resistance happens when the body does not respond properly to insulin. It can can raise a childs risk for type 2 ... What Is Insulin Resistance?. Insulin resistance happens when the body doesnt respond to the hormone insulin as it should, ... Who Gets Insulin Resistance?. Insulin resistance is most common in people who are overweight and have too much belly fat. ... Obesity and insulin resistance tends to run in families. Other things that put someone at risk for insulin resistance include: ...
The same insulin resistance that leads to type 2 diabetes is also linked to heart problems. Heres why managing diabetes helps ... Insulin Resistance and Your Heart. Insulin resistance means your body isnt using the hormone insulin the right way. Insulin ... Insulin Resistance and Heart Diseases. Insulin resistance and diabetes can cause many types of heart-related conditions. Heart ... "Insulin Resistance.". Cardiovascular Diabetology: "Association between insulin resistance and the development of cardiovascular ...
Aside from medication, changing certain lifestyle factors can improve insulin resistance. ... Insulin resistance often goes unnoticed in the initial stages when an individual is described as prediabetic. If the condition ... changing certain lifestyle factors can improve insulin resistance. In general, treatment of insulin resistance involves:. ... Insulin Resistance Treatment. News-Medical, viewed 18 November 2019, https://www.news-medical.net/health/Insulin-Resistance- ...
This cellular uptake of glucose is facilitated by the hormone insulin, which is secreted by the beta cells of the pancreas. ... Insulin also helps convert excess glucose into glycogen for storage in the liver. ... In people with insulin resistance, the muscles, fat and liver cells fail to respond to insulin in this way and glucose remains ... This insulin resistance and hyperglycemia can lead to type 2 diabetes and metabolic syndrome. Metabolic syndrome is ...
Insulin resistance occurs when the body doesnt respond as well to the insulin that the pancreas is making and glucose is less ... Insulin Resistance. Someone with type 2 diabetes still produces insulin, but the body just doesnt respond to insulin normally ... and the persons pancreas isnt able to make enough extra insulin to overcome this insulin resistance. Insulin resistance ... People who have insulin resistance may or may not develop type 2 diabetes. ...
... a marker of insulin resistance) and fasting insulin levels compared with baseline. No difference between ezetimibe/simvastatin ... Simvastatin/Ezetimibe on Parameters of Insulin Resistance. E. Moutzouri; E. Liberopoulos; D. P. Mikhailidis; M. S. Kostapanos; ... The primary end point was changes in homeostasis model assessment of insulin resistance (HOMA-IR). Secondary endpoints ... was associated with a dosedependent increase in insulin resistance.[6,7] Ezetimibe is a cholesterol absorption inhibitor, which ...
Causes of insulin resistance include metabolic syndrome, pregnancy, stress, obesity, and inactivity. Risk factors, diet ... Insulin resistance is a condition that is a precursor to developing type 2 diabetes. ... Exercise may help prevent insulin resistance. *Insulin resistance may be part of the metabolic syndrome, and it has been ... Insulin resistance precedes the development of type 2 diabetes (T2D).. *The causes of insulin resistance include both genetic ( ...
In this MNT Knowledge Center article, learn about how to reduce insulin insensitivity and the risk of type 2 diabetes. Which ... Insulin resistance has a close relationship with the development of blood sugar management and diabetes. ... Insulin resistance makes cells less sensitive to insulin. This means the body has to produce more insulin to keep blood sugar ... So what is insulin resistance and how might it link to weight? Can insulin resistance be reversed and what lifestyle changes ...
Learn about the causes of insulin resistance and prediabetes, how prediabetes is diagnosed, and steps you can take to help ... What is insulin resistance?. Insulin resistance is when cells in your muscles, fat, and liver dont respond well to insulin and ... What causes insulin resistance and prediabetes?. Researchers dont fully understand what causes insulin resistance and ... How do doctors diagnose insulin resistance and prediabetes?. *How can I prevent or reverse insulin resistance and prediabetes? ...
... a condition in which the bodys tissues and organs do not respond properly to the hormone insulin. Explore symptoms, ... Type A insulin resistance syndrome is a rare disorder characterized by severe insulin resistance, ... Type A insulin resistance syndrome is a rare disorder characterized by severe insulin resistance, a condition in which the ... Type A insulin resistance syndrome is one of a group of related conditions described as inherited severe insulin resistance ...
Systemic insulin resistance produces a proatherogenic lipid phenotype. Early in the course of systemic insulin resistance, FFAs ... Systemic insulin resistance, which increases levels of glucose and lipids, is not desirable. However, insulin resistance in ... Beneficial vascular interventions in insulin resistance. *Rationale for modulating insulin resistance to treat atherosclerosis ... More direct support for the involvement of insulin resistance in atherosclerosis came from the Insulin Resistance ...
Insulin resistance in obesity and type 2 diabetes.. The term "insulin resistance" usually connotes resistance to the effects of ... On diabetes: insulin resistance * Series Introduction: The molecular and physiological basis of insulin resistance: emerging ... The significance of the location of body fat for insulin resistance.. The relationship between obesity and insulin resistance ... and the major basis for this link is the ability of obesity to engender insulin resistance. Insulin resistance is a fundamental ...
Insulin resistance is a state in which a given concentration of insulin produces a less-than-expected biological effect. (See ... Age distribution for insulin resistance. Type A insulin resistance typically occurs in younger patients, while type B insulin ... Prevalence of insulin resistance by race. Insulin resistance syndrome is found in all races. The degree of clustering of the ... Specific causes of insulin resistance. Specific conditions and agents that may cause insulin resistance include the following: ...
... sometimes occurs in diabetic dogs. Insulin resistance is typically identified when a dog receiving a ... Insulin resistance may also be indicated by the dogs need to receive substantially increased amounts of insulin in order to ... Ruling out Insulin Resistance. Just because your diabetic dogs insulin may have become ineffective, doesnt automatically mean ... Weight gain can also cause insulin resistance. Excessive weight can block the insulin receptors, making it difficult for the ...
Insulin Resistance. Although most cats respond favorably to insulin, few develop insulin resistance, which occurs due to bodily ... The insulin dosage will then be altered in order to determine if the cat is really suffering from insulin resistance. ... The vet will have to re-examine pets that dont respond to insulin or develop insulin resistance, to choose a treatment option ... However, newer forms of insulin reduce the pets susceptibility to insulin resistance caused by antibodies. ...
Pessin, J. E., & Saltiel, A. R. (2000). Signaling pathways in insulin action: Molecular targets of insulin resistance. The ... Boura-Halfon, S., & Zick, Y. (2009). Phosphorylation of IRS proteins, insulin action, and insulin resistance. American Journal ... IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. ... 2002). Diet-induced insulin resistance in mice lacking adiponectin/ACRP30. Nature Medicine, 8, 731-737.PubMedCrossRef ...
... A. H. Dédjan, A. Chadli, S. El Aziz, and A. Farouqi ... M. Veilleux-Lemieux and A. D. DiVasta, "Severe hyperandrogenemia and insulin resistance in a 12-year-old girl," Journal of ... R. L. Barbieri and K. J. Ryan, "Hyperandrogenism, insulin resistance, and acanthosis nigricans syndrome: a common ...
I did a ton of research on the condition and found that insulin resistance is common among women ... What Is Insulin Resistance?. Insulin Resistance Is the Precursor to Diabetes You May Not Even Realize You Have April 18, 2018 ... "Most people who are obese are insulin resistant," she said. Other than the likelihood of having insulin resistance from being ... I tapped a few experts to weight in on what exactly insulin resistance is and how it can be treated. The good news: an insulin ...
"Insulin resistance induced by high glucose and high insulin precedes insulin receptor substrate 1 protein depletion in human ... M. D. Michael, R. N. Kulkarni, C. Postic et al., "Loss of insulin signaling in hepatocytes leads to severe insulin resistance ... "Muscle insulin resistance in uremic humans: glucose transport, glucose transporters, and insulin receptors," American Journal ... β-induced insulin receptor substrate-1 dysfunction and insulin resistance in rat models of diabetes and obesity," Kidney ...
The recognition of insulin resistance in patients who were not receiving insulin awaited the introduction of 1) the insulin ... Insulin resistance at the level of the β-cell, coupled with peripheral insulin resistance, might provide a unifying hypothesis ... Insulin resistance is associated with continuous exposure to high levels of insulin. Regardless of whether the insulin ... Insulin resistance was initially recognized in insulin-treated patients who required larger than usual doses of insulin. ...
Processed foods are the primary culprits causing insulin resistance; doctors are finally starting to talk about the food ... insulin resistance, which is exceedingly prevalent in the U.S.37,38 Insulin resistance, in turn, is a diet-induced condition. ... insulin resistance, which is exceedingly prevalent in the U.S. Insulin resistance, is a diet-induced condition. ... Insulin Resistance Is the Real Pandemic. So, to summarize, the real pandemic here appears to be dysregulated glucose metabolism ...
By this definition, it may pertain to many biological actions of insulin in many tissues of the body. Typically, however, in ... Insulin resistance can be broadly defined as a subnormal biological response to normal insulin concentrations. ... Immunologic reactions to insulin: insulin allergy, insulin resistance, and the autoimmune insulin syndrome. Diabetes Care 1979 ... and the spectrum of clinical disorders in which insulin resistance plays a major role has changed markedly. Insulin resistance ...
... revealing that insulin resistance is a product of decreased insulin-stimulated skeletal muscle glycogen synthesis, which can ... Etiology of insulin resistance.. Petersen KF1, Shulman GI.. Author information. 1. Department of Internal Medicine, Howard ... The hypothesis that insulin resistance is a result of accumulation of intracellular lipid metabolites (e.g., fatty acyl CoAs, ... The mechanism of fatty acid-induced insulin resistance in muscle (A) and liver (B). GLUT 4 = glucose transporter 4; IRS = ...
... fat and liver that respond significantly to insulin, said Kahn. Studying insulin resistance as it progresses through pre- ... "There have been no good human cell models to study insulin resistance, but such cells can now be made with iPSCs," said Kahn, ... In one line of research, Kahn added, the Joslin team will examine how much of insulin resistance in type 2 diabetes is genetic ... Until now, scientists examining the causes and effects of insulin resistance have struggled with a general lack of human cell ...
In the development of insulin resistance, the researchers dont think SeP acts on its own. It is well known, they explain, that ... Further studies in mice added support to the notion that the connection between SeP and insulin resistance is causal. When the ... Researchers have identified a hormone produced and secreted by the liver as a previously unknown cause of insulin resistance. ... the liver might contribute to the development of type 2 diabetes and insulin resistance via secretory proteins they call " ...
  • Magnesium supplementation has been used as a preventive approach in type 2 diabetes by improving insulin sensitivity. (news-medical.net)
  • Based on the significant improvement in insulin sensitivity in humans after bariatric surgery and rats with surgical removal of the duodenum, [18] [19] it has been proposed that some substance is produced in the mucosa of that initial portion of the small intestine that signals body cells to become insulin resistant. (wikipedia.org)
  • Over time, cells stop responding to all that insulin-they've become insulin resistant. (cdc.gov)
  • How do you find out if you're insulin resistant? (cdc.gov)
  • They also are more likely to be insulin resistant if obese or of Latino, African-American, Native American, or Asian-American heritage. (medicinenet.com)
  • Insulin resistance (IR) is a condition in which the body's cells become resistant to the effects of insulin. (medicinenet.com)
  • The syndromes of insulin resistance actually make up a broad clinical spectrum, which includes obesity, glucose intolerance, diabetes, and the metabolic syndrome, as well as an extreme insulin-resistant state. (medscape.com)
  • 2012). Apelin treatment increases complete fatty acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice. (springer.com)
  • Most people who are obese are insulin resistant," she said. (popsugar.com)
  • Finally, recent MRS studies in healthy, lean, elderly subjects and lean insulin-resistant offspring of parents with type 2 diabetes have demonstrated that reduced mitochondrial activity may also lead to increased intramyocellular lipid content and insulin resistance in skeletal muscle in these individuals. (nih.gov)
  • Now, the researchers report the results of comprehensive gene expression analyses, revealing that the liver expresses higher levels of the gene encoding selenoprotein P (SeP) in people with type 2 diabetes who are more insulin resistant. (redorbit.com)
  • When the researchers gave normal mice SeP, they became insulin resistant and their blood sugar levels rose. (redorbit.com)
  • What makes the cells resistant to the insulin or "insulin resistant? (healthcentral.com)
  • In fact, a 2002 study showed that 32.2% of the US population may be insulin resistant ( 1 ). (healthline.com)
  • In other words, they become "resistant" to the insulin. (healthline.com)
  • The cells become increasingly more insulin resistant, and both insulin and blood sugar levels go up. (healthline.com)
  • If you are insulin resistant, then you have low insulin sensitivity. (healthline.com)
  • Being insulin resistant is a bad thing, while being insulin sensitive is good. (healthline.com)
  • However, normal weight or thin people can also be insulin resistant, it is just much more common among those who are overweight ( 19 ). (healthline.com)
  • Virtually all patients with type 2 diabetes are insulin resistant, and the insulin-resistant status normally precedes the onset of diabetes by 1 to 2 decades ( 2 , 3 ). (diabetesjournals.org)
  • When the body produces insulin under conditions of insulin resistance, the cells are resistant to the insulin and are unable to use it as effectively, leading to high blood sugar . (wikipedia.org)
  • It also shows that insulin induces substantial expression and secretion of MCP-1 both in vitro in insulin-resistant (IR) 3T3-L1 adipocytes and in vivo in IR obese mice ( ob / ob ). (pnas.org)
  • The degree to which the other actions of insulin (e.g., gene expression) remain normal or become resistant in type II diabetes is not clear. (pnas.org)
  • Interestingly, these studies also reveal that insulin-resistant (IR) adipocytes and mice remained sensitive to insulin in terms of PAI-1 gene expression, possibly because glucose homeostasis and PAI-1 gene expression are regulated by different insulin signaling pathways ( 13 ). (pnas.org)
  • The presentation of insulin resistance depends on the type and stage of the insulin-resistant state. (medscape.com)
  • Most patients have one or more clinical features of the insulin-resistant state. (medscape.com)
  • When people are insulin resistant, their muscle, fat, and liver cells do not respond properly to insulin. (scdhec.gov)
  • If you are insulin resistant then your insulin levels are elevated all the time. (healthstatus.com)
  • Prolonged fasting can also make you insulin resistant. (healthstatus.com)
  • We have identified molecular and functional characteristics of insulin resistant subjects and distinctions between TZD treatment responder and nonresponder subjects. (pnas.org)
  • Insulin resistant subjects exhibited alterations in skeletal muscle (e.g., glycolytic flux and intramuscular adipocytes) and adipose tissue (e.g., mitochondrial metabolism and inflammation) that improved relative to TZD-induced insulin sensitization. (pnas.org)
  • Pre-TZD treatment expression of MLXIP in muscle and HLA-DRB1 in adipose tissue from insulin resistant subjects was linearly predictive of post-TZD insulin sensitization. (pnas.org)
  • We have conducted a mechanistic analysis of the gene expression profiles of adipose tissue (AT) and skeletal muscle (SM) from 72 subjects ranging from insulin-sensitive to insulin-resistant. (pnas.org)
  • Insulin resistant subjects responded to TZD treatment with varied improvements in insulin sensitivity. (pnas.org)
  • We ranked the insulin resistant subjects by their degree of TZD response (i.e., increased insulin sensitivity based on rate of glucose disposal during the hyperinsulinemic-euglycemic clamp) to define responder and nonresponder subgroups. (pnas.org)
  • In a third model, they inserted an extra copy of the PKC-delta gene in the liver of 129 mice, which became much more insulin resistant and diabetic. (redorbit.com)
  • Insulin-mediated glucose disposal varies widely in apparently healthy human beings, and the more insulin resistant an individual, the more insulin they must secrete in order to prevent the development of type 2 diabetes. (nih.gov)
  • More recently, studies have shown that the prevalence of insulin resistance/hyperinsulinemia is increased in patients with nonalcoholic fatty liver disease, and there are reports that certain forms of cancer are more likely to occur in insulin resistant/hyperinsulinemic persons. (nih.gov)
  • Evidence is also accumulating that sympathetic nervous system (SNS) activity is increased in insulin resistant, hyperinsulinemic individuals, and, along with the salt sensitivity associated with insulin resistance/hyperinsulinemia, increases the likelihood that these individuals will develop essential hypertension. (nih.gov)
  • The first step in the process of atherogenesis is the binding of mononuclear cells to the endothelium, and mononuclear cells isolated from insulin resistant/hyperinsulinemic individuals adhere with greater avidity. (nih.gov)
  • Further evidence of the relationship between insulin resistance and endothelial dysfunction is the finding that asymmetric dimethylarginine, an endogenous inhibitor of the enzyme nitric oxide synthase, is increased in insulin resistant/hyperinsulinemic individuals. (nih.gov)
  • Finally, plasma concentrations of several inflammatory markers are elevated in insulin resistant subjects. (nih.gov)
  • Depending on the levels of this enzyme, some mice can eat more and be less active, but still won't become insulin resistant, thus maintaining a healthy weight. (medpagetoday.com)
  • But then the study's authors go on to say that this knowledge "may prove useful in the future development of new therapeutic approaches for the treatment of insulin resistant diseases. (mendosa.com)
  • What Should A Woman Do If She Thinks She Might Be Insulin Resistant? (empowher.com)
  • The determination of insulin in serum is primarily used for the diagnosis of glycemic disorders in diabetic and pre-diabetic patients in the assessment of insulin resistant syndromes. (questdiagnostics.com)
  • This study cannot rule out the possibility that insulin-resistant children ingest food with higher phthalate content, or that insulin-resistant children excrete more DEHP. (aappublications.org)
  • However, the rats eating the high-fat diet with BCAA became as insulin resistant as rats fed a high-fat only diet, even though they weren't eating as much. (medicalnewstoday.com)
  • Insulin resistant subjects and type 2 diabetic patients are characterized by a decreased metabolic flexibility: a reduced capability to switch from fat oxidation in the basal state to carbohydrate oxidation in the insulin-stimulated state. (clinicaltrials.gov)
  • Insulin-resistant people have trouble absorbing glucose, or blood sugar. (menshealth.com)
  • Although most women with gestational diabetes do not remain diabetic right after delivery, they do commonly remain resistant to their insulin, and 30 to 50 percent of them develop type 2 diabetes within a few years after pregnancy. (scienceblog.com)
  • But when cells grow resistant to insulin, beta cells must create more insulin to make up that resistance. (scienceblog.com)
  • If you are insulin resistant, your body might produce insulin, but your body just can't seem to use it. (medical-supplies-equipment-company.com)
  • Only 23 subjects, about half insulin resistant, half not, stuck it out until the end. (jax.org)
  • Also, the researchers observed differences in the metabolomics profiles of the insulin resistant (IR) versus insulin sensitive (IS) individuals. (jax.org)
  • As many as one quarter of all Americans may be insulin resistant. (empowher.com)
  • A glucose tolerance test can determine if someone is insulin resistant or not. (diabetesnet.com)
  • Most people who are insulin resistant still produce enough insulin to maintain a normal blood glucose level. (diabetesnet.com)
  • Signs of low-grade systemic inflammation are not uncommon among people who have the pre-diabetic condition known as metabolic syndrome, as well as in animal models of obesity and type 2, or insulin-resistant, diabetes, said senior author H. Henry Dong, Ph.D., assistant professor, Department of Pediatrics, University of Pittsburgh School of Medicine. (eurekalert.org)
  • In the current paper, the researchers found in cultured cells and mouse experiments that Fox01 stimulates inflammatory white blood cells called macrophages, which migrate to the liver and adipose, or fat, tissue in insulin-resistant states, to increase production of a cytokine called interleukin-1 beta (IL-1B). (eurekalert.org)
  • The findings suggest that when there is a lack of insulin or when cells such as macrophages are resistant to its presence, there are no brakes on Fox01's stimulation of IL-1B and its further interference with insulin signaling," Dr. Dong said. (eurekalert.org)
  • In type 2 diabetes, the body becomes resistant to the effect of insulin, leading to elevated blood sugar levels. (eurekalert.org)
  • Dyslipidemia in insulin resistant individuals is characterized by elevated triglycerides, apolipoprotein B, small dense low density lipoprotein (LDL) particles, and reduced high density lipoprotein (HDL) concentration and smaller HDL particle size. (mdpi.com)
  • These findings are supported by pre-clinical and clinical studies that have shown improvements in insulin resistance (i.e., increased insulin sensitivity) after obese and insulin-resistant rodents or humans consumed blueberries. (mdpi.com)
  • however, it is possible to be insulin resistant without being overweight or obese. (diabetes.co.uk)
  • When the body becomes resistant to insulin, it tries to cope by producing more insulin. (diabetes.co.uk)
  • Based on the significant improvement in insulin sensitivity in humans after bariatric surgery and rats with surgical removal of the duodenum, it has been proposed that some substance is produced in the mucosa of that initial portion of the small intestine that signals body cells to become insulin resistant. (wikipedia.org)
  • Insulin is released by the pancreas in response to carbohydrates consumed in the diet. (wikipedia.org)
  • Even though the pancreas is still making insulin, the body doesn't let insulin do its job as well and it's harder for glucose to get into the cells. (kidshealth.org)
  • Blood sugar enters your bloodstream, which signals the pancreas to release insulin. (cdc.gov)
  • The pancreas pumps out more insulin to get blood sugar into cells. (cdc.gov)
  • The pancreas keeps making more insulin to try to make cells respond. (cdc.gov)
  • This cellular uptake of glucose is facilitated by the hormone insulin, which is secreted by the beta cells of the pancreas. (news-medical.net)
  • Someone with type 2 diabetes still produces insulin, but the body just doesn't respond to insulin normally and the person's pancreas isn't able to make enough extra insulin to overcome this insulin resistance. (kidshealth.org)
  • Insulin resistance occurs when the body doesn't respond as well to the insulin that the pancreas is making and glucose is less able to enter the cells. (kidshealth.org)
  • Insulin is a hormone produced by the beta cells of the pancreas. (medicinenet.com)
  • As a result, higher levels of insulin are needed in order for insulin to have its proper effects, and the pancreas compensates by trying to produce more insulin. (medicinenet.com)
  • With insulin resistance, the pancreas produces more and more insulin until the pancreas can no longer produce sufficient insulin for the body's demands, and then blood sugar rises. (medicinenet.com)
  • The pancreas releases insulin to help the body absorb glucose and maintain healthy blood sugar levels. (medicalnewstoday.com)
  • The pancreas secretes insulin into the bloodstream. (medicalnewstoday.com)
  • If the pancreas is unable to keep up with the increased demand for insulin, blood sugar levels go up. (medicalnewstoday.com)
  • Carbohydrates that have a high GI can cause blood sugar spikes and put more demand on the pancreas to make insulin. (medicalnewstoday.com)
  • Insulin is a hormone made by the pancreas that helps glucose in your blood enter cells in your muscle, fat, and liver, where it's used for energy. (nih.gov)
  • When blood glucose, also called blood sugar, levels rise after you eat, your pancreas releases insulin into the blood. (nih.gov)
  • As a result, your pancreas makes more insulin to help glucose enter your cells. (nih.gov)
  • As long as your pancreas can make enough insulin to overcome your cells' weak response to insulin, your blood glucose levels will stay in the healthy range. (nih.gov)
  • Prediabetes usually occurs in people who already have some insulin resistance or whose beta cells in the pancreas aren't making enough insulin to keep blood glucose in the normal range. (nih.gov)
  • Cat diabetes occurs when the pancreas doesn't produce sufficient insulin or if the body doesn't respond appropriately to the amount of insulin produced. (vetinfo.com)
  • Insulin is a hormone secreted by the pancreas to help digest carbohydrates to glucose, so that your cells can absorb glucose to use as energy. (popsugar.com)
  • Insulin is a hormone that is produced by your pancreas. (healthcentral.com)
  • The pancreas contains little clusters of cells called islets and beta cells in the islets produce the insulin. (healthcentral.com)
  • Your pancreas can start to work overtime, with the beta cells putting out higher levels of insulin because it senses that the body's cells are resisting the insulin and not unlocking to utilize the available glucose. (healthcentral.com)
  • Initially the extra insulin may help, but ultimately the pancreas becomes over-worked and over time may start to put out less and less insulin (beta cells become exhausted), especially as the insulin resistance persists. (healthcentral.com)
  • Insulin is a hormone secreted by an organ called the pancreas. (healthline.com)
  • This is sensed by the cells in the pancreas, which then release insulin into the blood. (healthline.com)
  • When this happens, the pancreas start producing even more insulin to bring the blood sugar levels down. (healthline.com)
  • The pancreas releases the hormone insulin into the bloodstream to help convert glucose, which comes from food, into energy. (livestrong.com)
  • High blood glucose and excessive insulin secretion can damage the pancreas and cause Type 2 diabetes. (livestrong.com)
  • This slower process does not put a sudden demand on the pancreas to release lots of insulin, so blood sugar increases gradually and in a regulated fashion. (livestrong.com)
  • Beta cells in the pancreas subsequently increase their production of insulin, further contributing to a high blood insulin level. (wikipedia.org)
  • Insulin, a hormone made by the pancreas, helps the body use glucose for energy. (scdhec.gov)
  • As the blood glucose level rises after a meal, the pancreas releases insulin to help cells take in and use the glucose. (scdhec.gov)
  • The pancreas tries to keep up with this increased demand for insulin by producing more. (scdhec.gov)
  • Eventually, the pancreas fails to keep up with the body's need for insulin. (scdhec.gov)
  • Type 2 diabetes is sometimes defined as the form of diabetes that develops when the body does not respond properly to insulin, as opposed to type 1 diabetes, in which the pancreas makes little or no insulin. (scdhec.gov)
  • Your body sends a signal to your pancreas to produce insulin. (healthstatus.com)
  • HFLC diet effect on pancreas, insulin resistance and beta cells in mice. (diabetesdaily.com)
  • Insulin resistance happens when insulin , released by the beta cells in the pancreas, doesn't work normally to stimulate glucose uptake into tissues. (medicalnewstoday.com)
  • Type 1 diabetes most often occurs before the age of 20 years and involves progressive destruction of insulin-producing cells in the pancreas. (yourhealthbase.com)
  • Insulin is released by the pancreas in response to the presence of sugar (glucose) in the blood stream. (yourhealthbase.com)
  • As a result, the pancreas either becomes exhausted trying to produce extra insulin, (leading to diabetes) or else the body suffers from excessively high levels of insulin (leading to obesity, and increased risk of heart disease). (sparkpeople.com)
  • Insulin is a hormone produced by the pancreas that instructs cells (in the muscle, fat and liver) to take up glucose (sugar) from the blood stream when there is too much glucose in the blood. (medmovie.com)
  • The pancreas responds by making more insulin to try to keep blood glucose levels normal. (medmovie.com)
  • The insulin producing cells of the pancreas slowly become defective and eventually reduce in number. (medmovie.com)
  • Insulin resistance occurs when the body has trouble using the insulin it produces, thus causing metabolic disruptions in insulin signaling in the body such as the liver, muscles, the pancreas, and adipose (stored fat) tissue as well as in the hypothalamus of the brain. (drsears.com)
  • Insulin resistance causes the pancreas to release too much insulin (hyperinsulinemia). (wellspan.org)
  • The more a person weighs, the more insulin his or her pancreas makes and the less the person's body cells respond to insulin. (wellspan.org)
  • METS-IR also predicts visceral fat content, subcutaneous adipose tissue, fasting insulin levels and ectopic fat accumulation in liver and pancreas. (wikipedia.org)
  • Insulin resistance is considered a component of the metabolic syndrome . (wikipedia.org)
  • This insulin resistance and hyperglycemia can lead to type 2 diabetes and metabolic syndrome. (news-medical.net)
  • Insulin resistance may be part of the metabolic syndrome , and it has been associated with higher risk of developing heart disease . (medicinenet.com)
  • Considerable evidence supports the association between insulin resistance and vascular disease, and this has led to wide acceptance of the clustering of hyperlipidemia, glucose intolerance, hypertension, and obesity as a clinical entity, the metabolic syndrome. (jci.org)
  • While insulin resistance, by promoting dyslipidemia and other metabolic abnormalities, is part of the proatherogenic milieu, it is possible that insulin resistance itself in the vascular wall does not promote atherosclerosis. (jci.org)
  • Most likely, the pathways that mediate insulin's metabolic effects diverge downstream of PI3K ( 7 , 9 ) and show differential sensitivity to varying levels of insulin. (jci.org)
  • Preserved Na/HCO 3 cotransporter sensitivity to insulin may promote hypertension in metabolic syndrome," Kidney International , vol. 87, no. 3, pp. 535-542, 2015. (hindawi.com)
  • Insulin resistance, recently recognized as a strong predictor of disease in adults, has become the leading element of the metabolic syndrome and renewed as a focus of research. (diabetesjournals.org)
  • Insulin resistance has been assigned a central place in the metabolic disturbances associated with obesity and type 2 diabetes. (diabetesjournals.org)
  • were crystallized and brought to fruition by Reaven ( 1 ), who proposed in 1988 that the cluster of insulin resistance (and by definition, hyperinsulinemia), impaired glucose tolerance, abnormalities of plasma lipids, and hypertension were part of a single syndrome, Syndrome X. It has also been called the insulin resistance syndrome, the deadly quartet, and more commonly, the metabolic syndrome. (diabetesjournals.org)
  • See 'The metabolic syndrome (insulin resistance syndrome or syndrome X)' and 'Clinical manifestations of polycystic ovary syndrome in adults' and 'Ovarian hyperthecosis' . (uptodate.com)
  • [1] In theory, insulin resistance should even be strengthened under harsh metabolic conditions such as pregnancy, during which the expanding fetal brain demands more glucose. (wikipedia.org)
  • Obesity frequently is accompanied by related metabolic perturbations such as dyslipidemia, hypertension, insulin resistance, hyperinsulinemia, and the development of a procoagulant state, and these changes contribute to an increased risk for cardiovascular diseases ( 2 ). (pnas.org)
  • Collectively, these observations raise the possibility that in the situation of metabolic insulin resistance accompanied by hyperinsulinemia, the expression of certain insulin-responding genes may dramatically increase in insulin target tissues. (pnas.org)
  • Metabolic syndrome (syndrome X) - Note that a patient with the metabolic syndrome may be asymptomatic in spite of the presence of some, or even most, of the components of insulin resistance syndrome. (medscape.com)
  • Having several of these problems is called metabolic syndrome or insulin resistance syndrome, formerly called syndrome X. (scdhec.gov)
  • Estimates suggest that in Westernized countries 25-35 percent of the population have a degree of insulin resistance and the health consequences associated with this metabolic derangement. (chiro.org)
  • Central or abdominal obesity has been reported to have such a close association with insulin resistance that it is often now viewed as a clinical marker for this metabolic dysregulation. (chiro.org)
  • A clustering of metabolic problems associated with insulin resistance, including elevated plasma glucose, lipid regulation problems (elevated triglycerides, increased small low-density lipoproteins, and decreased high-density lipoproteins), high blood pressure, a prothrombic state, and obesity (especially central obesity) occurs commonly together. (chiro.org)
  • And, while insulin resistance might lie at the heart of the problem, all of these metabolic disorders appear to be closely related and can, together or independently, contribute to health problems. (chiro.org)
  • The stark reality is that a majority of people with this metabolic problem developed insulin resistance as a result of a lifetime of cumulative poor choices. (chiro.org)
  • Although there are certainly genetic factors contributing to this metabolic state, since the above factors are all modifiable to a greater or lesser degree, insulin resistance is potentially preventable. (chiro.org)
  • Some of the factors to consider when designing a diet for an individual with insulin resistance include age, underlying disease or metabolic conditions, activity level, vegetable content of the diet, and types of dietary fat and carbohydrates consumed. (chiro.org)
  • Insulin resistance is a defining feature of the metabolic syndrome and the primary defect leading to type 2 diabetes ( 1 , 2 ). (pnas.org)
  • We can show in animal models and in humans that it's insulin resistance in different tissues that creates many of the features of the metabolic syndrome," he told MedPage Today . (medpagetoday.com)
  • He's shown that expression in the liver of the enzyme PKC-delta determined whether animals were susceptible to insulin resistance and, subsequently, factors of metabolic syndrome. (medpagetoday.com)
  • on genetic manipulation shows that you can redirect or prevent the development of insulin resistance and metabolic syndrome, so be it. (medpagetoday.com)
  • These observations have prompted investigators to speculate that the accumulation of lipids in tissues not suited for fat storage (e.g., skeletal muscle and liver) is an underlying component of insulin resistance and the metabolic syndrome. (nih.gov)
  • We review the metabolic fates of lipids in insulin-responsive tissues and discuss the roles of specific lipid metabolites (e.g., ceramides, GM3 ganglioside, and diacylglycerol) as antagonists of insulin signaling and action. (nih.gov)
  • A:Insulin resistance (IR) is an independent risk factor for the development of metabolic syndrome and type 2 diabetes. (aacc.org)
  • The problem is, the metabolic pathways that result in insulin resistance are very complex and no drug-based treatment has yet been discovered. (diabetesdaily.com)
  • Next the team will study what happens when obese people who have insulin resistance lose weight and 'whether there is a parallel improvement in the BCAA metabolic signature in the blood,' Newgard said. (medicalnewstoday.com)
  • To provide more direct insight into the effect of carnitine in preventing metabolic inflexibility and insulin resistance and to further explore the mechanism of action is the focus of this research. (clinicaltrials.gov)
  • Objective: The primary objectives are to investigate whether L-carnitine infusion may rescue lipid-induced insulin resistance and whether L-carnitine infusion is improving metabolic flexibility in the state of lipid-induced insulin resistance. (clinicaltrials.gov)
  • To investigate whether L-Carnitine infusion may rescue lipid induced insulin resistance and improve metabolic flexibility three intervention trials are included. (clinicaltrials.gov)
  • But while it's well-known that obesity is the most common cause of insulin resistance - the primary metabolic abnormality in type 2 diabetes - researchers have only recently begun to effectively parse the underlying, complicated relationships between lipids (fats and related molecules essential to cell structure and function) and chronic tissue inflammation (a key cause of obesity-induced insulin resistance). (ucsd.edu)
  • A study reports that low blood protein levels are found to be associated with reduced insulin resistance and thus risk of diabetes , metabolic syndrome and cardiovascular disease decreased. (medindia.net)
  • Diabetes is a metabolic disease caused by insulin deficiency that leads to high blood sugar levels and several associated complications if left untreated. (medindia.net)
  • But diabetics, or people with insulin resistance (metabolic syndrome, syndrome X) whose bodies don't use insulin efficiently, would do well to get familiar with the glycemic index. (empowher.com)
  • Syndrome X, which is also known as the "metabolic syndrome" or "Insulin Resistance Syndrome", is a condition that is linked to an increased risk of diabetes and heart disease. (diabetesnet.com)
  • The metabolic effect of the insulin was then evaluated. (diabeteshealth.com)
  • The burden of obesity has increased globally over the last few decades and its association with insulin resistance and related cardio-metabolic problems have adversely affected our ability to reduce population morbidity and mortality. (mdpi.com)
  • Therapeutic lifestyle change continues to be the most important intervention in clinical practice to improve adipose tissue function and avoid development of insulin resistance and related cardio-metabolic complications. (mdpi.com)
  • Insulin resistance is an underlying key pathophysiologic process in the development of cardio-metabolic disorders among obese individuals. (mdpi.com)
  • High plasma levels of insulin and glucose due to insulin resistance are believed to be the origin of metabolic syndrome and type 2 diabetes, including its complications. (phys.org)
  • To evaluate the presence of insulin resistance and its association with other metabolic abnormalities in obese children and adolescents. (scielo.br)
  • The results confirmed that insulin resistance is present in many obese children and adolescents, and that this condition is associated with alterations that represent an increased risk for developing metabolic disorders in adulthood. (scielo.br)
  • Insulin resistance is the core metabolic disorder associated with type 2 diabetes. (medmovie.com)
  • Insulin resistance develops when its target cells in the body are having difficultt receiving appropriate metabolic instructions from insulin once it interacts with its receptor on the cell surface. (drsears.com)
  • The metabolic syndrome includes abdominal obesity, insulin resistance, high blood pressure, abnormal lipid levels, and possible cardiovascular disease. (rainbow.coop)
  • Sedentary lifestyle increases the likelihood of development of insulin resistance. (wikipedia.org)
  • Diabetes is an endocrine disorder and other endocrine disorders can lead to the development of insulin resistance. (vetinfo.com)
  • In the development of insulin resistance, the researchers don't think SeP acts on its own. (redorbit.com)
  • It is well known, they explain, that fat tissue is a main contributor to the development of insulin resistance by producing fat-derived hormones called adipokines. (redorbit.com)
  • What's more, an imbalance in the amount and type of gut microbiota is linked to the development of insulin resistance and obesity, according to the review. (livestrong.com)
  • Although the molecular mechanisms leading to development of insulin resistance also are not fully understood, there appears to be an association between insulin resistance and both the accumulation of abdominal visceral fat ( 4 ) and the presence of specific genetic components ( 5 ). (pnas.org)
  • Tumor necrosis factor α (TNF-α) is also elevated in obesity and may contribute to many aspects of adipose tissue biology including development of insulin resistance and abnormalities in lipid metabolism ( 11 ). (pnas.org)
  • Researchers at Joslin Diabetes Center have now identified an enzyme called PKC-delta as an important molecular modifier for development of insulin resistance, diabetes and fatty liver in mice. (redorbit.com)
  • Traditionally, adipose tissue in the visceral fat depot has been considered a major culprit in the development of insulin resistance. (mdpi.com)
  • However, there is a growing body of evidence supporting the role of subcutaneous truncal/abdominal adipose tissue in the development of insulin resistance. (mdpi.com)
  • However, it is not known whether plasma aldosterone levels predict the development of insulin resistance. (ahajournals.org)
  • 0.05) relative risk (1.71 [95% CI: 1.03-2.84]) was observed in the highest tertile versus lowest tertile of plasma aldosterone for the development of insulin resistance, after adjustment for confounding factors. (ahajournals.org)
  • This 10-year prospective study demonstrated that plasma aldosterone levels predicted the development of insulin resistance in a general population. (ahajournals.org)
  • 15 Accordingly, we conducted a longitudinal study in subjects in a general population without insulin resistance at baseline to clarify the relationship between circulating aldosterone levels and development of insulin resistance. (ahajournals.org)
  • Mechanisms of estradiol-induced insulin secretion by the G protein-coupled estrogen receptor GPR30/GPER in pancreatic beta-cells. (medscape.com)
  • This gene provides instructions for making a protein called an insulin receptor, which is found in many types of cells. (medlineplus.gov)
  • Most of the INSR gene mutations that cause type A insulin resistance syndrome lead to the production of a faulty insulin receptor that cannot transmit signals properly. (medlineplus.gov)
  • instead, it results from an abnormality of the immune system that blocks insulin receptor function. (medlineplus.gov)
  • The initial molecular signal for insulin action involves activation of the insulin receptor tyrosine kinase, which results in phosphorylation of insulin receptor substrates (IRSs) on multiple tyrosine residues. (jci.org)
  • Ambient insulin levels, various physiologic and disease states, and drugs regulate insulin receptor concentration or affinity. (medscape.com)
  • L. J. Hale and R. J. Coward, "The insulin receptor and the kidney," Current Opinion in Nephrology and Hypertension , vol. 22, pp. 100-106, 2013. (hindawi.com)
  • Glomerular-specific protein kinase C- β -induced insulin receptor substrate-1 dysfunction and insulin resistance in rat models of diabetes and obesity," Kidney International , vol. 79, no. 8, pp. 883-896, 2011. (hindawi.com)
  • Par14 protein associates with insulin receptor substrate 1 (IRS-1), thereby enhancing insulin-induced IRS-1," The Journal of Biological Chemistry , vol. 288, no. 28, pp. 20692-20701, 2013. (hindawi.com)
  • Role of the insulin receptor substrate 1 and phosphatidylinositol 3-kinase signaling pathway in insulin-induced expression of sterol regulatory element binding protein 1c and glucokinase genes in rat hepatocytes," Diabetes , vol. 51, no. 6, pp. 1672-1680, 2002. (hindawi.com)
  • J. Landis and L. M. Shaw, "Insulin receptor substrate 2-mediated phosphatidylinositol 3-kinase signaling selectively inhibits glycogen synthase kinase 3 β to regulate aerobic glycolysis," The Journal of Biological Chemistry , vol. 289, no. 26, pp. 18603-18613, 2014. (hindawi.com)
  • This defect appears to be a result of intracellular lipid-induced inhibition of insulin-stimulated insulin-receptor substrate (IRS)-1 tyrosine phosphorylation resulting in reduced IRS-1-associated phosphatidyl inositol 3 kinase activity. (nih.gov)
  • Kahn and his colleagues used fibroblasts from three patients with severe insulin resistance brought on by mutations in the gene for the insulin receptor (IR), a molecule that crosses the cell membrane and plays a key role in insulin signaling and glucose metabolism. (harvard.edu)
  • The elevated MCP-1 may alter adipocyte function because addition of MCP-1 to differentiated adipocytes in vitro decreases insulin-stimulated glucose uptake and the expression of several adipogenic genes ( LpL, adipsin, GLUT-4, aP2 , β3-adrenergic receptor, and peroxisome proliferator-activated receptor γ). (pnas.org)
  • Hypoglycemia results from interaction between insulinomimetic antibodies and the insulin receptor. (medscape.com)
  • Receptor and post-receptor defects contribute to the insulin resistance in non-insulin dependent diabetes mellitus. (springer.com)
  • Role of human skeletal muscle insulin receptor kinase in the in vivo insulin resistance of noninsulin dependent diabetes mellitus and obesity. (springer.com)
  • Omega-3 fats activate this macrophage receptor with broad anti-inflammatory effects and improved insulin sensitivity. (mendosa.com)
  • Congenital factors like fetal undernutrition and ethnic differences can lead to IR, as can molecular defects such as genetic mutations that cause insulin receptor defects or post-binding signaling. (aacc.org)
  • 2 Aldosterone induces hypokalemia, which may modulate insulin secretion, has direct effects on insulin receptor function, 3 , 4 causes pancreatic β-cell dysfunction or even apoptosis, 5 interferes with insulin signaling pathways, 6 and decreases insulin sensitivity in human adipocytes in vitro. (ahajournals.org)
  • 7 Moreover, aldosterone reduces the expression of insulin-sensitizing factors, such as adiponectin and peroxisome proliferator-activated receptor-γ, in obese, diabetic mice. (ahajournals.org)
  • 10 , 11 Moreover, insulin resistance was restored by surgical intervention or mineralocorticoid receptor blocker in primary hyperaldosteronism. (ahajournals.org)
  • The potential role of vitamin D deficiency in insulin resistance has been proposed to be associated with inherited gene polymorphisms including vitamin D-binding protein, vitamin D receptor, and vitamin D 1alpha-hydroxylase gene. (scribd.com)
  • With these activations, an impairment of the insulin signaling is observed, with decreased phosphorylation of the insulin receptor, insulin receptor substrate (IRS) and Akt, as well as increased inhibitory serine phosphorylation of IRS-1. (mdpi.com)
  • Several lines of evidence have demonstrated that insulin and the insulin receptor play a key role in the formation and progression of breast cancer. (knowcancer.com)
  • Some people with insulin resistance may also need to take metformin . (webmd.com)
  • In people with insulin resistance, the muscles, fat and liver cells fail to respond to insulin in this way and glucose remains in the blood rather than being taken up, even when insulin levels are raised. (news-medical.net)
  • People with insulin resistance are often diagnosed with prediabetes. (medicalnewstoday.com)
  • Unlike most people with insulin resistance, females with type A insulin resistance syndrome are usually not overweight. (medlineplus.gov)
  • Long before people with insulin resistance develop abnormalities of glucose metabolism, circulating FFA levels increase. (jci.org)
  • Many people with insulin resistance have high levels of both glucose and insulin circulating in their blood at the same time. (scdhec.gov)
  • Many people with insulin resistance and high blood glucose have other conditions that increase the risk of developing type 2 diabetes and damage to the heart and blood vessels, also called cardiovascular disease. (scdhec.gov)
  • In addition, the insulin resistance correlated with increased fat in the liver, an increasing problem in people with insulin resistance. (redorbit.com)
  • People with insulin resistance are at a high risk of getting type 2 diabetes . (health24.com)
  • People with insulin resistance are often producing too more insulin than healthy people. (diabetes.co.uk)
  • There are a number of risk factors for insulin resistance, including being overweight or obese or having a sedentary lifestyle . (wikipedia.org)
  • Doctors might think it's insulin resistance if an overweight or obese person has acanthosis nigricans or a family history of diabetes or heart disease. (kidshealth.org)
  • In obese humans and rodent models, the expression of pro-inflammatory adipokines is enhanced and can directly result in insulin resistance. (springer.com)
  • And while people who have insulin resistance aren't necessarily more prone to gaining weight, being overweight or obese can cause insulin resistance, explained Kathleen Wyne, MD, endocrinologist at The Ohio State University Wexner Medical Center. (popsugar.com)
  • Other than the likelihood of having insulin resistance from being overweight or obese, the only other physical symptom is acanthosis nigricans , or a dark coloring of the skin on the neck or armpit. (popsugar.com)
  • Characterization of selective resistance to insulin signaling in the vasculature of obese Zucker (fa/fa) rats," The Journal of Clinical Investigation , vol. 104, no. 4, pp. 447-457, 1999. (hindawi.com)
  • A treatment that blocked the activity of SeP in the livers of diabetic and obese mice improved their sensitivity to insulin and lowered blood sugar levels. (redorbit.com)
  • About a third of obese children and teenagers may also have insulin resistance ( 4 ). (healthline.com)
  • Studies of genetically obese mice and cultured adipocytes demonstrate that insulin and TNF-α are two mediators that regulate PAI-1 expression in the adipocyte in vivo ( 12 ). (pnas.org)
  • The Argentinian investigators examined the association between insulin resistance and the following indexes: waist circumference, BMI, waist circumference/height, weight/(sitting height)(2), and waist circumference/sitting height of 625 children, 91 of whom were overweight and another 96 of whom were classified as obese. (medscape.com)
  • Conversely, deletion of NE in obese mice fed a high-fat diet improved insulin sensitivity. (ucsd.edu)
  • One in five American adolescents are obese, and many of these patients exhibit some level of insulin resistance (IR). (bioportfolio.com)
  • A University of Sao Paulo study of 135 individuals, half with normal weight and the other half obese, suggests there is a link between obesity and the body's inability to use insulin-insulin resistance. (diabeteshealth.com)
  • A clue about the blood chemistry of obese people who develop insulin resistance , a precursor to diabetes , has been confirmed in animal studies at the Duke University Medical Center. (medicalnewstoday.com)
  • To determine whether the BCAA signature in obese humans might signal that their intake is harmful, the scientists performed a feeding study in rats that showed an independent contribution of BCAAs to insulin resistance. (medicalnewstoday.com)
  • Because obese humans tend to ingest high-fat diets, the combination of high-BCAA and high-fat intake might contribute to insulin resistance in obese humans, but additional studies are needed. (medicalnewstoday.com)
  • The main known causes of insulin resistance syndrome are a combination of genetic factors, obesity (about 50-60 percent of women with PCOS are obese), and insufficient physical exercise. (sparkpeople.com)
  • The most effective way to improve insulin resistance in overweight and obese people, is through a combination of weight loss and increased physical activity. (sparkpeople.com)
  • Figure 4: Intraduodenal resveratrol improves insulin sensitivity in obese rats and lowers HGP and plasma glucose levels in hyperglycemic rats. (nature.com)
  • Insulin assay standardization: leading to measures of insulin sensitivity and secretion for practical clinical care. (medscape.com)
  • Secondary endpoints consisted of changes in fasting insulin levels, fasting plasma glucose (FPG), glycosylated haemoglobin (HbA 1c ), the HOMA of b-cell function (HOMA-B) (a marker of basal insulin secretion by pancreatic b-cells), LDL-C and high sensitivity C reactive protein (hsCRP). (medscape.com)
  • thus, insulin resistance results in increased insulin secretion to maintain normal glucose and lipid homeostasis. (medscape.com)
  • GLP-1 is an incretin hormone that stimulates insulin secretion, causes B-cell mitosis while inhibiting apoptosis, inhibits glucagon secretion, and delays gastric emptying with overall antidiabetic effects. (medscape.com)
  • the liver participates in the pathogenesis of insulin resistance through hormone secretion," said Hirofumi Misu of Kanazawa University Graduate School of Medical Science in Japan. (redorbit.com)
  • 1 Although fasting insulin is a reasonable measure of insulin resistance, it is potentially confounded by variability in insulin secretion. (ahajournals.org)
  • Some proposed mechanisms for this effect include weight gain, decreased insulin secretion from pancreatic beta cells and insulin resistance. (mercola.com)
  • TZDs enhance insulin sensitivity by improving glucose and lipid metabolism, altering adipokine secretion, and reducing adipose tissue inflammation ( 4 , 8 ). (pnas.org)
  • Bogardus C, Lillioja S, Howard BV, Reaven G, Mott D. Relationships between insulin secretion, insulin action, and fasting plasma glucose concentration in non-diabetic and non-insulindependent diabetic subjects. (springer.com)
  • Ward WK, Beard JC, Halter JB, Pfeifer MA, Porte D Jr. Pathophysiology of insulin secretion in non-insulin-dependent diabetes mellitus. (springer.com)
  • DeFronzo RA, Tobin JD, Andres R. Glucose clamp technique: a method for quantifying insulin secretion and resistance. (springer.com)
  • The incidence of type 2 DM is increasing worldwide and results from a lack of insulin or inadequate insulin secretion following increases in insulin resistance. (scribd.com)
  • Dietary factors likely contribute to insulin resistance, however, causative foods are difficult to determine given the limitations of nutrition research. (wikipedia.org)
  • Some medications can contribute to insulin resistance. (medicinenet.com)
  • Obesity, especially central belly fat, is believed to contribute to insulin resistance because the fat seems to cause inflammation that disrupts insulin's effectiveness. (healthcentral.com)
  • In some cases an autoimmune process can contribute to insulin resistance. (healthcentral.com)
  • Excess weight and lack of physical activity also contribute to insulin resistance. (scdhec.gov)
  • The suspicion has been that these amino acids, in combination with a high-fat diet, contribute to insulin resistance. (medicalnewstoday.com)
  • Statin drugs contribute to insulin resistance in human subjects. (greenmedinfo.com)
  • Failure of liver cells to respond to insulin by converting glucose to glycogen, means glycogen stores are also decreased. (news-medical.net)
  • Although most cats respond favorably to insulin, few develop insulin resistance, which occurs due to bodily changes or inability of the body to respond to insulin. (vetinfo.com)
  • The vet will have to re-examine pets that don't respond to insulin or develop insulin resistance, to choose a treatment option that works effectively to control diabetes. (vetinfo.com)
  • It's thought that reducing the activity of SHIP2 will restore the ability of cells to respond to insulin. (diabetes.org.uk)
  • And that boosting the activity of C5aR improves the way muscle cells respond to insulin, so that the cells can better take up glucose from the blood. (diabetes.org.uk)
  • The team then want to see whether targeting C5aR could help people with or at risk of type 2 diabetes lose weight and improve how their bodies respond to insulin. (diabetes.org.uk)
  • In insulin resistance, cells of the body do not respond to insulin to efficiently remove glucose. (medmovie.com)
  • Insulin resistance is a state where the body does not respond to insulin as well as it should. (diabetes.co.uk)
  • There are multiple ways to measure insulin resistance such as fasting insulin levels or glucose tolerance tests but these are not often used in clinical practice. (wikipedia.org)
  • They first assessed the patients' baseline insulin resistance using the homeostasis model assessment (HOMA), calculated using fasting blood glucose and fasting insulin levels. (topnews.in)
  • There are also grounds for considering the related possibility that insulin resistance and hyperinsulinemia, in addition to being caused by obesity, can contribute to the development of obesity. (jci.org)
  • however, only in the early stages of impaired insulin metabolism do hyperglycemia and hyperinsulinemia appear to be significant contributors to the presence of hypertension. (medscape.com)
  • Thus, insulin resistance is by definition tethered to hyperinsulinemia. (diabetesjournals.org)
  • 3 ) Rats and humans treated with escalating doses of insulin show both hyperinsulinemia and insulin resistance. (diabetesjournals.org)
  • In summary, hyperinsulinemia is often both a result and a driver of insulin resistance. (diabetesjournals.org)
  • This leads to high insulin levels in the blood, termed hyperinsulinemia. (healthline.com)
  • Therefore, the causal role of insulin resistance/compensatory hyperinsulinemia in the development of hypertension continues to be debated. (ahajournals.org)
  • The hyperinsulinemia that frequently accompanies obesity and insulin resistance may therefore contribute to the altered expression of these and other genes in insulin target tissues. (pnas.org)
  • However, the combination of insulin resistance and compensatory hyperinsulinemia increases the likelihood that an individual will be hypertensive, and have a dyslipidemia characterized by a high plasma triglyceride (TG) and low high-density lipoprotein cholesterol (HDL-C) concentration. (nih.gov)
  • These changes increase risk of cardiovascular disease (CVD), and in 1988, this cluster of related abnormalities was designated as comprising a syndrome (X). Several other clinical syndromes are now known to be associated with insulin resistance and compensatory hyperinsulinemia. (nih.gov)
  • For example, polycystic ovary syndrome appears to be secondary to insulin resistance and compensatory hyperinsulinemia. (nih.gov)
  • Finally, there is substantial evidence of an association between insulin resistance/hyperinsulinemia, and sleep disordered breathing. (nih.gov)
  • Given the rapid increase in the number of clinical syndromes and abnormalities associated with insulin resistance/hyperinsulinemia, it seems reasonable to suggest that the cluster of these changes related to the defect in insulin action be subsumed under the term of the insulin resistance syndrome. (nih.gov)
  • In addition to the identification of additional clinical syndromes related to insulin resistance/hyperinsulinemia, a number of new risk factors have been recognized that would increase CVD risk in these individuals. (nih.gov)
  • Elevated plasma concentrations of plasminogen activator inhibitor-1 (PAI-1) have been shown to be associated with increased CVD, and there is evidence of a significant relationship between PAI-1 and fibrinogen levels and both insulin resistance and hyperinsulinemia. (nih.gov)
  • It is obvious that the cluster of abnormalities associated with insulin resistance and compensatory hyperinsulinemia contains many well-recognized CVD risk factors, choosing which one, or ones, that are primarily responsible for the accelerated atherogenesis that characterizes this syndrome is not a simple task. (nih.gov)
  • Experimental studies show that insulin has growth promoting effects on pancreatic cancer cells and patients with type 2 diabetes mellitus are known to exhibit hyperinsulinemia, during the early stages of their disease. (rxpgnews.com)
  • It's important to note that insulin resistance, hyperinsulinemia, and insulin insensitivity is not common to all patients with polycystic ovary syndrome. (sparkpeople.com)
  • If you have a mild or moderate form of insulin resistance, blood tests may show normal or high blood glucose (hyperglycemia) and high levels of insulin (hyperinsulinemia) at the same time. (medmovie.com)
  • [1] Various genetic factors can increase risk, such as a family history of diabetes, and there are some specific medical conditions associated with insulin resistance, such as polycystic ovary syndrome . (wikipedia.org)
  • 2 Recently, depression was found to be associated with greater insulin resistance in women with polycystic ovary syndrome. (bmj.com)
  • Polycystic ovary syndrome and non-alcoholic fatty liver disease (NAFLD) are associated with insulin resistance. (wikipedia.org)
  • This severe resistance to the effects of insulin impairs blood sugar regulation and leads to diabetes mellitus. (medlineplus.gov)
  • Pleiotropic effects of insulin to promote adipose storage. (jci.org)
  • Until now, scientists examining the causes and effects of insulin resistance have struggled with a general lack of human cell lines from tissues such as muscle, fat and liver that respond significantly to insulin, said Kahn. (harvard.edu)
  • One biologically plausible mechanism whereby type 2 diabetes mellitus may be related to pancreatic carcinogenesis is through the growth-regulatory effects of insulin. (rxpgnews.com)
  • Insulin resistance in fat cells reduces the effects of insulin and results in elevated hydrolysis of stored triglycerides in the absence of measures which either increase insulin sensitivity or which provide additional insulin. (phys.org)
  • Insulin resistance (IR) occurs when a person's metabolism resists the effects of insulin, and the person is unable to handle sugar intake normally. (rainbow.coop)
  • It is certainly possible to reduce the effects of insulin resistance and there are a number of effective ways to do this. (diabetes.co.uk)
  • Likewise, you won't know if you have most of the other conditions that are part of insulin resistance syndrome ( high blood pressure , low "good" cholesterol levels, and high triglycerides) without seeing your doctor. (webmd.com)
  • Type A insulin resistance syndrome is a rare disorder characterized by severe insulin resistance, a condition in which the body's tissues and organs do not respond properly to the hormone insulin. (medlineplus.gov)
  • In people with type A insulin resistance syndrome, insulin resistance impairs blood sugar regulation and ultimately leads to a condition called diabetes mellitus, in which blood sugar levels can become dangerously high. (medlineplus.gov)
  • Severe insulin resistance also underlies the other signs and symptoms of type A insulin resistance syndrome. (medlineplus.gov)
  • The features of type A insulin resistance syndrome are more subtle in affected males. (medlineplus.gov)
  • Type A insulin resistance syndrome is one of a group of related conditions described as inherited severe insulin resistance syndromes. (medlineplus.gov)
  • Type A insulin resistance syndrome represents the mildest end of the spectrum: its features often do not become apparent until puberty or later, and it is generally not life-threatening. (medlineplus.gov)
  • Type A insulin resistance syndrome is estimated to affect about 1 in 100,000 people worldwide. (medlineplus.gov)
  • Type A insulin resistance syndrome results from mutations in the INSR gene. (medlineplus.gov)
  • This condition is designated as type A to distinguish it from type B insulin resistance syndrome. (medlineplus.gov)
  • Type A insulin resistance syndrome can have either an autosomal dominant or, less commonly, an autosomal recessive pattern of inheritance. (medlineplus.gov)
  • Associations with low HDL cholesterol and hypertension followed, and Reaven integrated this information in his 1988 Banting Lecture ( 6 ) when he coined the term "syndrome X" for the insulin resistance syndrome. (jci.org)
  • In clinical practice, no single laboratory test is used to diagnose insulin resistance syndrome. (medscape.com)
  • When I was diagnosed with polycystic ovarian syndrome (PCOS), I did a ton of research on the condition and found that insulin resistance is common among women who have PCOS. (popsugar.com)
  • The present application describes a composition that includes an extract of Gynostemma pentaphyllum used to treat insulin resistance syndrome, obesity, hypertriglyceridemia, as well as decrease body fat mass. (freepatentsonline.com)
  • 4. A method for treating symptoms of insulin resistance syndrome, obesity/overweight and hypertriglyceridemia in a subject administering to the subject a therapeutically effective amount of the composition according to claim 1. (freepatentsonline.com)
  • 7. A method for treating symptoms of insulin resistance syndrome, obesity/overweight, decreasing body fat mass and hypertriglyceridemia in a subject comprising administering to the subject a therapeutically effective amount of gypenosides composition from the composition according to claim 1. (freepatentsonline.com)
  • Central obesity, not peripherally distributed fat, is a strong marker of insulin resistance syndrome. (medscape.com)
  • Waist or waist-to-hip ratio, height, weight, and body mass index (BMI) may indicate insulin resistance syndrome. (medscape.com)
  • Now, for some people, this insulin resistance syndrome doesn't really seem to mean anything to their health at first. (medical-supplies-equipment-company.com)
  • A diagnosis of the Insulin Resistance Syndrome is established when 3 or more of these risk factors are present. (diabetesnet.com)
  • Many women with PCOS have insulin resistance syndrome. (sparkpeople.com)
  • Excess weight may lead to insulin resistance, which in turn may play a part in the development of fatty liver disease . (nih.gov)
  • Administration of drugs such as prednisone, cortisone or glucocorticoids such as dexamethasone can interfere with insulin absorption or reduce the effectiveness of insulin and lead to insulin resistance. (vetinfo.com)
  • Increased oxidative stress and inflammation in the body may lead to insulin resistance ( 23 , 24 ). (healthline.com)
  • However, the mechanisms by which TZD-induced gene expression changes lead to insulin sensitization or by which TZD-induced insulin sensitization is prevented are poorly understood. (pnas.org)
  • Our rat studies show that this overload causes changes at the cellular level that can lead to insulin resistance. (medicalnewstoday.com)
  • New evidence suggests that obesity can cause this system to become overactive, and this in turn might lead to insulin resistance - a key feature of type 2 diabetes. (diabetes.org.uk)
  • In contrast to agonism of PPAR-gamma, phosphorylation has a narrow effect, disrupting a smaller set of genes that lead to insulin resistance. (scienceblog.com)
  • Whilst the exact cause of insulin resistance is still not fully understood, it is well-known which factors can lead to insulin resistance developing. (diabetes.co.uk)
  • Lemon detox diet reduced body fat, insulin resistance, and serum hs-CRP level without hematological changes in overweight Korean women. (nih.gov)
  • We investigated anthropometric indices, insulin sensitivity, levels of serum adipokines, and inflammatory markers in overweight Korean women before and after clinical intervention trial. (nih.gov)
  • It isn't clear exactly what causes insulin resistance, but a family history of type 2 diabetes, being overweight (especially around the waist), and being inactive all can raise the risk. (cdc.gov)
  • You do not have to be overweight to have insulin resistance. (cdc.gov)
  • Insulin resistance is most common in people who are overweight and have too much belly fat. (kidshealth.org)
  • A variety of genetic and environmental factors are thought to raise the risk of insulin resistance but being overweight and physically inactive are major causative contributors. (news-medical.net)
  • Being overweight or having obesity are risk factors for developing insulin resistance or prediabetes. (nih.gov)
  • Scientists haven't pinned down the exact cause, but they believe being overweight and sedentary are major contributors to insulin resistance. (livestrong.com)
  • Insulin sensitivity was not significantly related to hypertension in older or overweight participants or in participants with baseline BP ≥130/85 mm Hg. (ahajournals.org)
  • For that, we will study free radicals production, inflammatory markers, adipokines, mitochondrial function, insulin sensitivity and energy substrate utilization in healthy volunteers at risk for insulin resistance and T2D (1st degree relatives of T2D patients with associated overweight). (clinicaltrials.gov)
  • Even so, experts consider that normalizing insulin response may reduce PCOS symptoms like obesity or severe overweight, erratic periods, excessive body and facial hair, and acne, as well as improving the risk of heart disease and diabetes in the process. (sparkpeople.com)
  • People who are overweight mostly in the upper body have greater insulin resistance and have the greatest risk for type 2 diabetes. (wellspan.org)
  • Insulin also signals the liver to store blood sugar for later use. (cdc.gov)
  • Lower insulin levels alert the liver to release stored blood sugar so energy is always available, even if you haven't eaten for a while. (cdc.gov)
  • There's lots of insulin, too, telling the liver and muscles to store blood sugar. (cdc.gov)
  • Insulin also helps convert excess glucose into glycogen for storage in the liver. (news-medical.net)
  • Insulin resistance is when cells in your muscles, fat, and liver don't respond well to insulin and can't easily take up glucose from your blood. (nih.gov)
  • Disorders such as kidney disease, liver disease or pancreatitis can cause the body to release hormones that cause the insulin given to be less effective in processing blood sugars. (vetinfo.com)
  • In addition, pets treated with medication for underlying conditions such as hyperthyroidism, liver disease or pancreatitis may also develop insulin resistance. (vetinfo.com)
  • Deletion of Gab1 in the liver leads to enhanced glucose tolerance and improved hepatic insulin action. (springer.com)
  • Alternative causes of insulin resistance (IR) mediated via fat accumulation in skeletal muscle and liver. (nih.gov)
  • Researchers have identified a hormone produced and secreted by the liver as a previously unknown cause of insulin resistance. (redorbit.com)
  • On the basis of those findings, Misu and colleagues began to suspect that, similar to the role of fat tissue, the liver might contribute to the development of type 2 diabetes and insulin resistance via secretory proteins they call "hepatokines. (redorbit.com)
  • Insulin helps your body's muscle, fat and liver cells access the sugar which provides energy to the cells. (healthcentral.com)
  • Insulin also helps your liver and muscle tissue to store excess glucose. (healthcentral.com)
  • Insulin can also signal the liver to produce less glucose. (healthcentral.com)
  • Eating in a way that balances your blood sugar, reduces inflammation and oxidative stress , and improves your liver detoxification is the key to preventing and reversing insulin resistance and diabetes. (huffingtonpost.com)
  • Because the muscles, liver and cells can't use the insulin effectively, glucose builds up in the bloodstream. (livestrong.com)
  • Fructose, which is metabolised into triglycerides in the liver, stimulates insulin production through another mechanism, and can have a more potent effect than other carbohydrates. (wikipedia.org)
  • Although insulin resistance, by definition, describes an impaired biological responsiveness to insulin, it is frequently used to describe a defect in insulin-stimulated glucose uptake by muscle and adipocytes and/or a decrease in gluconeogenesis by the liver. (pnas.org)
  • Consistent with this hypothesis, Shimomura and colleagues ( 14 ) demonstrated that in murine leptin-deficient states insulin signaling in the liver also diverges along two pathways and they showed that the transcription factor SREBP-1c is another gene that remains sensitive to insulin in these IR mice. (pnas.org)
  • Using liver and fat cells from mice and humans and live mouse models, a team led by Jerrold M. Olefsky, MD, associate dean for scientific affairs at UC San Diego Health Sciences and professor of medicine, discovered that an enzyme secreted by neutrophils called neutrophil elastase (NE) impairs insulin signaling and boosts resistance. (ucsd.edu)
  • NE degrades IRS1, a key protein in the insulin signaling pathway in both liver and fat cells. (ucsd.edu)
  • Although NE has been shown to degrade this protein in lung cancer cells, the scientists said, the effect on insulin target tissues such as liver and adipose is striking. (ucsd.edu)
  • 1 ] Insulin resistance means, in its simplest sense, that the ability of insulin to dispose of glucose in the liver, skeletal muscle, and other peripheral tissues is compromised. (chiro.org)
  • Insulin resistance is a pathological state in which insulin action is impaired in target tissues including liver, skeletal muscle, and adipose tissue. (pnas.org)
  • It comprises abnormalities in the pancreatic islets, the liver, and the peripheral insulin target tissues. (springer.com)
  • Cellular alterations in liver, skeletal muscle, and adipose tissue responsible for insulin resistance in obesity and Type II diabetes. (springer.com)
  • The resistance prevents muscle, fat, and liver cells from easily absorbing glucose. (topnews.in)
  • Insulin resistance (IR) is the condition in which normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells. (phys.org)
  • Insulin resistance in muscle cells reduces glucose uptake (and so local storage of glucose as glycogen), whereas insulin resistance in liver cells results in impaired glycogen synthesis and a failure to suppress glucose production. (phys.org)
  • Elevated blood fatty acid levels (associated with insulin resistance and diabetes mellitus Type 2), reduced muscle glucose uptake, and increased liver glucose production all contribute to elevated blood glucose levels. (phys.org)
  • We also found that the glucoregulatory role of duodenally acting resveratrol required activation of Sirt1 and AMP-activated protein kinase (Ampk) in this tissue to initiate a gut-brain-liver neuronal axis that improved hypothalamic insulin sensitivity and in turn, reduced HGP. (nature.com)
  • Insulin also helps muscles, fat, and liver cells store sugar to be released when it is needed. (wellspan.org)
  • Aside from medication, changing certain lifestyle factors can improve insulin resistance. (news-medical.net)
  • Medications such as metformin, exenatide and a class of drugs called the thiazolidinediones can help improve insulin resistance. (news-medical.net)
  • In addition to working out, losing weight will improve insulin resistance - losing just 15 pounds and keeping it off will slow the progression to diabetes, said Dr. Wyne. (popsugar.com)
  • Given that NE mediates insulin resistance, one could, in theory, take an NE activity inhibitory approach to reverse or improve insulin resistance," Oh said, noting that NE inhibitors are already used for treatment of emphysema in Japan and are being tested in the United States, both for emphysema and type 1 diabetes. (ucsd.edu)
  • This study lends support for more research to test the cognitive benefits of interventions such as exercise, diet, and medications that improve insulin resistance in order to prevent dementia," says Prof. Tanne. (topnews.in)
  • This hyperglycemia triggers the beta cells to produce even more insulin, raising the level of insulin further still. (news-medical.net)
  • The mice are of normal weight but show insulin resistance, hyperglycemia, and hypertriglyceridemia. (diabetesjournals.org)
  • 2 ) Somogyi described patients with unusually high doses of insulin and hyperglycemia. (diabetesjournals.org)
  • The term first came into use several years after the introduction of insulin therapy in 1922 to describe occasional diabetic patients who required increasingly large doses of insulin to control hyperglycemia. (uptodate.com)
  • Insulin resistance may arise from defects in fatty acid oxidation ( 7 ), and secondary β-cell lipotoxicity may contribute to defects in insulin resistance and hyperglycemia ( 8 ). (diabetesjournals.org)
  • To prevent hyperglycemia and noticeable organ damage over time, [2] the body produces insulin when glucose starts to be released into the bloodstream , primarily from the digestion of carbohydrates in the diet. (wikipedia.org)
  • Based on these results, the authors suggest combining antipsychotics with vitamin D supplementation to "efficaciously safeguard against antipsychotic-induced hyperglycemia accompanied by insulin resistance. (mercola.com)
  • Combination of hyperglycemia and virilization occurs in several syndromes of insulin resistance. (medscape.com)
  • Serum insulin assay: an important therapeutic tool in management of freshly diagnosed type 2 diabetes mellitus. (medscape.com)
  • Cat insulin is a synthetic form of insulin that's administered to cats suffering from diabetes mellitus. (vetinfo.com)
  • In normoglycemic subjects, fasting insulin correlated well with whole-body glucose uptake ( r =−0.68) as measured by the "gold standard" euglycemic hyperinsulinemic clamp method, although the correlation was lower in individuals with impaired glucose tolerance or type 2 diabetes mellitus. (ahajournals.org)
  • Although the role of insulin resistance in the pathophysiology of type 2 diabetes mellitus is well accepted, the relationship between insulin resistance and blood pressure remains controversial. (ahajournals.org)
  • Insulin action and insulin resistance in non-insulin dependent diabetes mellitus. (springer.com)
  • Dinneen S, Gerich J, Rizza R. Carbohydrate metabolism in non-insulin-dependent diabetes mellitus. (springer.com)
  • In conclusion, our results support the hypothesis that higher insulin concentrations and insulin resistance may be a mechanism that explains the associations between diabetes mellitus, higher glucose concentration, and pancreatic cancer observed in previous studies. (rxpgnews.com)
  • Biochemically defined diabetes mellitus and insulin concentration in the highest quartile demonstrated significant 2-fold increased risks. (rxpgnews.com)
  • However, research has shown that Asian Americans may have an increased risk for insulin resistance even without a high BMI. (nih.gov)
  • What Women Are At Risk For Insulin Resistance? (empowher.com)
  • Obesity and insulin resistance tends to run in families. (kidshealth.org)
  • BPA is positively associated with generalized obesity, abdominal obesity, and insulin resistance in middle-aged and elderly Chinese adults. (greenmedinfo.com)
  • But exactly how obesity and insulin resistance are linked to the complement system isn't fully understood. (diabetes.org.uk)
  • The development of obesity and insulin resistance has been extensively studied in the last decades, but the mechanisms underlying these alterations are still not completely understood. (mdpi.com)
  • What Are the Signs & Symptoms of Insulin Resistance? (kidshealth.org)
  • There are no specific signs and symptoms of insulin resistance. (medicinenet.com)
  • Other diet plans offer more specific ways to improve symptoms of insulin resistance. (medicalnewstoday.com)
  • 2 Since insulin resistance is positively associated with the development of diabetes, 1 we hypothesised-given that disturbed glucoregulatory functions behind the development of diabetes might be associated with pathophysiological changes in depression 2 -that insulin resistance should be positively correlated with depressive symptoms. (bmj.com)
  • 4 We defined insulin resistance with the qualitative insulin sensitivity check index, 4 and we evaluated the severity of depressive symptoms with Beck's depression inventory 21. (bmj.com)
  • Insulin resistance (a low qualitative insulin sensitivity check index) and severity of depressive symptoms (Beck's depression inventory 21) were positively correlated, particularly in people with impaired glucose tolerance. (bmj.com)
  • Fatigue, frequent urination, abnormal thirst, increased appetite, blurred vision, and slow healing of skin, gum and urinary infections are common symptoms of insulin resistance and type 2 diabetes. (yourhealthbase.com)
  • Furthermore, insulin disorders may be symptoms of more underlying causes. (sparkpeople.com)
  • Initially, insulin resistance presents no symptoms. (diabetes.co.uk)
  • Insulin resistance ( IR ) is a pathological condition in which cells fail to respond normally to the hormone insulin . (wikipedia.org)
  • Insulin resistance happens when the body doesn't respond to the hormone insulin as it should, making it hard for glucose to get into cells. (kidshealth.org)
  • Insulin resistance means your body isn't using the hormone insulin the right way. (webmd.com)
  • Insulin resistance implies that the cells are not responding well to the hormone insulin. (healthline.com)
  • Normally, after eating a meal, the resulting glucose-from-food is dispersed by the pancreatic hormone insulin to the cells for use as energy. (sparkpeople.com)
  • Insulin resistance is the name given to when cells of the body don't respond properly to the hormone insulin. (diabetes.co.uk)
  • Insulin signaling, through PI3K-dependent pathways, also promotes the degradation of apoB. (jci.org)
  • cellular actions of insulin involve a wide variety of effects on postreceptor signaling pathways within target cells. (medscape.com)
  • The scientists then looked at gene activation in insulin signaling pathways for iPSCs and fibroblasts with IR mutations, and for corresponding cells derived from people without those mutations. (harvard.edu)
  • This disrupts the signalling pathways needed for insulin to work ( 9 , 10 , 11 ). (healthline.com)
  • The team will look at the impact of reduced SHIP2 activity on chemical pathways that affect insulin signalling. (diabetes.org.uk)
  • We have uniquely characterized coordinated cellular and tissue functional pathways that are characteristic of insulin resistance, TZD-induced insulin sensitization, and potential TZD responsiveness. (pnas.org)
  • Macrophage infiltration in adipose tissue activates inflammatory pathways that induce insulin resistance and modulate the effects of adipose tissue on whole-body metabolism ( 5 ). (pnas.org)
  • Furthermore, a secondary objective is to examine the molecular pathways of carnitine and acetylcarnitine, responsible for muscle insulin sensitivity. (clinicaltrials.gov)
  • The best way to reverse [insulin resistance], if it's caught early enough, is through lifestyle modifications ," said Eduardo Grunvald, MD, program director at UC San Diego's Weight Management Program. (popsugar.com)
  • Avoiding carbohydrates and sugars, a no-carbohydrate diet or fasting can reverse insulin resistance. (wikipedia.org)
  • But you should also know that you can reverse insulin resistance in many cases. (medical-supplies-equipment-company.com)
  • Avandia and Actos belong to a relatively new class of compounds called thiazolidinediones, the first medications that can reverse insulin resistance. (scienceblog.com)
  • Together, these studies highlight the therapeutic relevance of targeting duodenal SIRT1 to reverse insulin resistance and improve glucose homeostasis in obesity and diabetes. (nature.com)
  • Various factors such as using a different syringe or faulty administration can change the body's response to insulin. (vetinfo.com)
  • These antibodies are the body's response to insulin medication, as it treats insulin like a foreign object and develops antibodies to combat insulin. (vetinfo.com)
  • The drugs act on a master regulatory protein called PPAR-gamma, primarily in fat cells, which governs genes involved in the body's response to insulin. (scienceblog.com)
  • Some medicines such glucocorticoids (for example, prednisone) can reduce the body's response to insulin. (wellspan.org)
  • factors related to stress, socio-economic status and history have been shown to activate the stress response, which increases the production of glucose and insulin resistance, as well as inhibiting pancreatic function and thus might be of importance, [13] [14] although it is not fully corroborated by the scientific evidence. (wikipedia.org)
  • Insulin is synthesized by the pancreatic beta cell as a precursor, proinsulin. (questdiagnostics.com)
  • By JAMA, Higher insulin concentrations and insulin resistance are associated with an increased risk of pancreatic cancer in men, according to a study in the December 14 issue of JAMA. (rxpgnews.com)
  • Rachael Z. Stolzenberg-Solomon, Ph.D., of the National Cancer Institute, Department of Health and Human Services, Rockville, Md., and colleagues examined a cohort from the ATBC study to determine whether fasting serum insulin and glucose concentrations were associated with risk for incident pancreatic cancer. (rxpgnews.com)
  • The researchers found that after adjustment for age, years smoked, and body mass index, higher concentrations of glucose, insulin, and insulin resistance tended to show positive dose-response associations with pancreatic cancer. (rxpgnews.com)
  • There were significant interactions between quartile-categorized glucose, insulin, and insulin resistance and pancreatic cancer by follow-up time, such that risks were greater among the cases that occurred with longer follow-up time. (rxpgnews.com)
  • Lifestyle changes to decrease glucose and insulin concentrations through weight reduction, increasing physical activity, and diet such as decreasing saturated fat intake, and identification of other modifiable factors that may contribute to higher glucose and insulin concentrations could possibly impact pancreatic cancer development, as well as other cancer and chronic disease," the researchers write. (rxpgnews.com)
  • Defects in pancreatic β-cell function, insulin sensitivity, and systemic inflammation all contribute to the development of type 2 DM. (scribd.com)
  • Vitamin D has in vitro and in vivo effects on pancreatic β-cells and insulin sensitivity. (scribd.com)
  • In insulin resistance, various clinical entities of this state are evident. (medscape.com)
  • The number of clinical events observed, as a function of insulin resistance tertile at baseline. (diabetesjournals.org)
  • Typically, however, in clinical practice, insulin resistance refers to a state in which a given concentration of insulin is associated with a subnormal glucose response [ 1 ]. (uptodate.com)
  • Antiinsulin antibodies are rare in patients treated with recombinant human insulin, and the spectrum of clinical disorders in which insulin resistance plays a major role has changed markedly. (uptodate.com)
  • Studying insulin resistance as it progresses through pre-clinical stages of type 2 diabetes has been particularly challenging. (harvard.edu)
  • Clinical data from humans and animals reveals honey supplementation reduces or improves insulin resistance, according to the "IJBS" review. (livestrong.com)
  • Thus, the indexes derived from fasting insulin and glucose, such as the Homeostasis Model Assessment (HOMA), 2 the Quantitative Insulin Sensitivity Check Index (QUICKI), 3 and the insulin sensitivity index (ISI) developed by Gutt and coworkers, 4 have been more widely used to assess insulin resistance in clinical and population-based studies. (ahajournals.org)
  • The subjects underwent multiple SM and AT biopsies, hyperinsulinemic-euglycemic clamps, 3-month treatment with an insulin-sensitizing TZD, and clinical characterization. (pnas.org)
  • Here we review encouraging preclinical and clinical data indicating the potential of targeting impaired insulin signaling with antidiabetic drugs to treat dementia. (frontiersin.org)
  • Given the role that insulin resistance plays in type 2 diabetes, using such data to predict changes in at-risk people is of potentially high clinical value. (jax.org)
  • 8 In addition to the above-mentioned in vitro and animal studies, several clinical studies reported an association between plasma aldosterone levels and insulin resistance. (ahajournals.org)
  • 14 Thus, some clinical studies suggest a causal relationship between aldosterone and insulin resistance, but others indicate that insulin sensitivity in primary aldosteronism is no worse than in essential hypertension. (ahajournals.org)
  • Insulin resistance and prediabetes occur when your body doesn't use insulin well. (nih.gov)
  • Who is more likely to develop insulin resistance or prediabetes? (nih.gov)
  • People who have genetic or lifestyle risk factors are more likely to develop insulin resistance or prediabetes. (nih.gov)
  • These lifestyle changes can lower your chances of developing insulin resistance or prediabetes. (nih.gov)
  • What causes insulin resistance and prediabetes? (nih.gov)
  • Researchers don't fully understand what causes insulin resistance and prediabetes, but they think excess weight and lack of physical activity are major factors. (nih.gov)
  • Not getting enough physical activity is linked to insulin resistance and prediabetes. (nih.gov)
  • In the early stages of insulin resistance and prediabetes, and sometimes even in the presence of Type 2 diabetes, weight loss can usually reverse the condition. (healthcentral.com)
  • This sets the stage for prediabetes and ultimately Type 2 diabetes, by placing never-ending pressure on your insulin-producing beta islet cells. (healthcentral.com)
  • People who develop type 2 diabetes usually pass through earlier stages of insulin resistance and prediabetes , although those often go undiagnosed. (wikipedia.org)
  • Without sufficient insulin, excess glucose builds up in the bloodstream, leading to prediabetes, diabetes, and other serious health disorders. (topnews.in)
  • Although insulin is present in the bloodstream, the defective receptors make it less able to exert its effects on cells and tissues. (medlineplus.gov)
  • The lack of appropriate insulin signaling, especially in peripheral tissues such as adipose cells, results in abnormal lipid metabolism that consistently produces a proatherogenic phenotype (Figure 1 ). (jci.org)
  • Collectively, these findings have suggested that obesity-induced insulin resistance may result, at least in part, from an imbalance in the production of pro- and anti-inflammatory adipokines at adipose tissues. (springer.com)
  • By this definition, it may pertain to many biological actions of insulin in many tissues of the body. (uptodate.com)
  • Insulin resistance refers to the reduction in insulin-mediated glucose uptake in insulin-sensitive tissues, specifically in skeletal muscle. (ahajournals.org)
  • This results in more inflammation in tissues that are important for glucose control, which means that they respond poorly to insulin.In people with Type 2, macrophages themselves also respond poorly to insulin, with harmful consequences. (diabetes.org.uk)
  • The key intersection among the three diseases is insulin resistance, which has been classically described to occur in peripheral tissues in diabetes and obesity and has recently been shown to develop in Alzheimer's disease (AD) brains. (frontiersin.org)
  • Insulin typically inhibits Fox01, setting up a feedback loop in healthy tissues that helps regulate insulin levels. (eurekalert.org)
  • Insulin resistance refers to the inability of the body tissues to respond properly to insulin . (wellspan.org)
  • If the body tissues do not respond properly to insulin, the blood sugar level rises. (wellspan.org)
  • Insulin resistance--mechanisms, syndromes, and implications. (medscape.com)
  • Insulin resistance is also linked to some genetic syndromes, conditions that affect hormone levels and stress levels, and some medicines. (kidshealth.org)
  • The mechanisms responsible for insulin resistance syndromes include genetic or primary target cell defects, autoantibodies to insulin, and accelerated insulin degradation. (medscape.com)
  • Blood sugar enters cells, and levels in the bloodstream decrease, signaling insulin to decrease too. (cdc.gov)
  • Without enough insulin, extra glucose stays in your bloodstream rather than entering your cells. (nih.gov)
  • Then insulin travels around the bloodstream, telling the body's cells that they should pick up sugar from the blood. (healthline.com)
  • Insulin is a vital hormone that signals your cells to absorb glucose from the bloodstream after a meal, making it crucial to blood sugar balance. (livestrong.com)
  • Insulin resistance is usually characterized by higher fasting and post-glucose loading insulin levels, and a decreased responsiveness of tissue to the insulin driven clearance of this glucose from the bloodstream. (chiro.org)
  • Laboratory tests include the plasma glucose level, the fasting insulin level, and a lipid profile, among others. (medscape.com)
  • The hypothesis that insulin resistance is a result of accumulation of intracellular lipid metabolites (e.g., fatty acyl CoAs, diacylglycerol) in skeletal muscle and hepatocytes is supported by observations in patients and mouse models of lipodystrophy. (nih.gov)
  • Insulin affects a number of biological processes including glucose transport, glucose/lipid metabolism, cell growth, protein synthesis, and gene expression ( 6 ). (pnas.org)
  • Impaired insulin-stimulated glucose uptake in skeletal muscle and lipid metabolism in adipocytes are central characteristics of insulin-resistance. (pnas.org)
  • Although TZDs improve insulin sensitivity and the glycemic, lipid, and inflammatory profiles of most patients, approximately 30% of diabetic subjects do not respond to TZD treatment, as gauged by fasting plasma glucose or HbA1c levels ( 9 , 10 ). (pnas.org)
  • Lipid abnormalities such as obesity, increased circulating free fatty acid levels, and excess intramyocellular lipid accumulation are frequently associated with insulin resistance. (nih.gov)
  • Here, we hypothesize that the capacity to form acetylcarnitine may rescue lipid-induced insulin resistance. (clinicaltrials.gov)
  • To this end, insulin resistance will be induced by lipid infusion in healthy volunteers and it will be tested whether carnitine co-infusion can alleviate insulin resistance. (clinicaltrials.gov)
  • MONMOUTH JUNCTION, N.J. - April 6, 2019 - PRLog -- Biotech Support Group reports on a recent patent application describing the simplicity and efficiency of their lipid clearance sample preparation technology for reducing analytical variables in liquid chromatography coupled to mass spectrophotometric (LC-MS) analysis of insulin and C-peptide. (prlog.org)
  • Serum insulin level, homeostasis model assessment insulin resistance scores, leptin, and adiponectin levels decreased in the Lemon-D and Positive-C groups. (nih.gov)
  • In states of insulin resistance, the same amount of insulin does not have the same effect on glucose transport and blood sugar levels. (wikipedia.org)
  • No one test will tell you, but if you have high blood sugar levels, high triglycerides (a kind of blood fat), high LDL ("bad") cholesterol, and low HDL ("good") cholesterol, your health care provider may determine you have insulin resistance. (cdc.gov)
  • Insulin resistance raises blood sugar levels, and high blood sugar leads to inflammation, which damages the lining inside arteries. (webmd.com)
  • Magnesium supplements administered daily can restore depleted levels of magnesium which can also improve the glucose uptake from blood mediated by insulin. (news-medical.net)
  • The test for insulin resistance is the measurement of fasting blood glucose and insulin levels. (medicinenet.com)
  • In individuals who will ultimately develop type 2 diabetes , research shows that blood glucose and insulin levels are normal for many years, until at some point in time, insulin resistance develops. (medicinenet.com)
  • High insulin levels are often associated with central obesity, cholesterol abnormalities, and/or high blood pressure ( hypertension ). (medicinenet.com)
  • Insulin is a hormone that helps the body absorb glucose, keeping blood sugar levels in balance. (medicalnewstoday.com)
  • Over time, insulin resistance can cause high blood sugar levels and damage cells. (medicalnewstoday.com)
  • This means the body has to produce more insulin to keep blood sugar levels healthy. (medicalnewstoday.com)
  • failure of the signals or of the B cells to adapt adequately in relation to insulin sensitivity results in inappropriate insulin levels, impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and type 2 diabetes. (medscape.com)
  • Insulin resistance is typically identified when a dog receiving a standard amount of insulin for his weight consistently has elevated blood sugar levels for the majority of the day. (vetinfo.com)
  • Insulin resistance may also be indicated by the dog's need to receive substantially increased amounts of insulin in order to keep his blood sugar levels under control. (vetinfo.com)
  • Excessive weight can block the insulin receptors, making it difficult for the insulin to effectively control blood sugar levels. (vetinfo.com)
  • Pets suffering from type 1 diabetes should also have a diet plan, as diets high in carbohydrates can reduce the effectiveness of insulin, causing pets to require higher dosages to keep the blood glucose levels normal. (vetinfo.com)
  • Although I knew that insulin resistance was related to elevated blood sugar levels and could lead to type 2 diabetes, I wasn't exactly sure what insulin resistance meant. (popsugar.com)
  • The condition exists when insulin levels are higher than expected relative to the level of glucose. (diabetesjournals.org)
  • 1 ) Mice transfected with extra copies of the insulin gene produce basal and stimulated insulin levels that are two to four times elevated. (diabetesjournals.org)
  • 5 ) Many patients with insulinoma who have elevated basal levels of insulin have reduced (but not absent) responsiveness to administered insulin. (diabetesjournals.org)
  • When insulin resistance occurs your blood sugar levels will remain persistently high. (healthcentral.com)
  • This causes higher insulin levels, higher blood sugar levels and may lead to type 2 diabetes and other health problems. (healthline.com)
  • Eat something every 4 hours to keep your insulin and glucose levels normal. (huffingtonpost.com)
  • It is most important to avoid eating quickly absorbed carbohydrates alone, as they raise your sugar and insulin levels. (huffingtonpost.com)
  • Insulin resistance is connected to obesity, hypertension and high levels of fat in the blood. (livestrong.com)
  • New research from the University of Alabama demonstrates that eating in an 8 hour window and then not eating the rest of the 24 hours lowered insulin levels, improved insulin sensitivity and lowered blood pressure. (healthstatus.com)
  • In short, PKC-delta levels correlated closely with insulin resistance and the abnormalities in glucose tolerance in all three cases of mice. (redorbit.com)
  • When we have insulin resistance, insulin doesn't regulate our blood glucose levels as well, and it often leads to type 2 diabetes. (mendosa.com)
  • Both insulin and C-peptide are released together from the beta cells in response to increased glucose levels. (questdiagnostics.com)
  • Because of differences in half-life and hepatic clearance, peripheral blood levels of C-peptide and insulin are no longer equimolar but remain highly correlated. (questdiagnostics.com)
  • Simple indices derived from fasting levels of glucose and insulin-especially the homeostasis model assessment and the quantitative insulin sensitivity check index-are the most commonly used tools for estimating IR. (aacc.org)
  • Additionally, biochemical markers such as fasting insulin, sex hormone binding globulin, and insulin-like growth factor binding protein 1 levels can provide useful information about IR status. (aacc.org)
  • The researchers also showed that BCAAs contributed to insulin resistance by chronically activating mTOR, a signaling protein that regulates cell growth and survival and that functions as a sensor of cellular nutrient and energy levels. (medicalnewstoday.com)
  • The researchers measured the insulin resistance of 489 coronary heart disease patients by calculating the insulin and glucose levels in their blood from 1990 to 1997. (menshealth.com)
  • but when they were put on pioglitazone during PIPOD, their blood sugar and insulin levels improved, and most significantly, their beta-cell function stabilized. (scienceblog.com)
  • Before starting to take pioglitazone, they tended to have lower glucose levels and slightly higher insulin levels and their beta cells seemed to compensate more strongly for insulin resistance. (scienceblog.com)
  • In the end, the patient with insulin resistance can have both high levels of sugar and of insulin the body instead of each 'canceling' the other out. (medical-supplies-equipment-company.com)
  • If the patient does not take active steps toward preventing and reversing insulin resistance, they can weaken their body so much that their blood sugar levels cause a diagnosis of type 2 diabetes. (medical-supplies-equipment-company.com)
  • Blood levels of c-reactive protein (CRP) and fasting insulin and glucose were also measured. (emaxhealth.com)
  • The researchers found that people with the highest levels of insulin resistance had twice as much PAD , regardless of other cardiovascular risk factors, including diabetes. (emaxhealth.com)
  • As a result, the body requires higher levels of insulin to usher glucose into its cells. (topnews.in)
  • Diabetes manifests itself through abnormally high blood glucose levels and comes in two major forms - insulin-dependent (type 1) and non-insulin-dependent (type 2). (yourhealthbase.com)
  • Cross-sectional studies have reported that plasma aldosterone levels are higher in patients with insulin resistance. (ahajournals.org)
  • We investigated the cross-sectional relationship between plasma aldosterone levels and insulin resistance (homeostasis model assessment index ≥1.73 according to the diagnostic criteria used in Japan) in 1088 nondiabetic participants. (ahajournals.org)
  • 9 Cross-sectional studies have shown an association between plasma aldosterone levels and insulin resistance in hypertensive and normotensive subjects. (ahajournals.org)
  • They found that excessive insulin levels were obvious in mice "as early as 1 month old. (pharmacytimes.com)
  • Other roles have been proposed to involve immunoregulatory function by activating innate and adaptive immunity and cytokine release, activating inflammation by upregulation of nuclear factor κB and inducing tumor necrosis factor α, and other molecular actions to maintain glucose homeostasis and mediate insulin sensitivity by a low calcium status, obesity, or by elevating serum levels of parathyroid hormone. (scribd.com)
  • We show here that acute intraduodenal infusion of resveratrol reversed a 3 d high fat diet (HFD)-induced reduction in duodenal-mucosal Sirt1 protein levels while also enhancing insulin sensitivity and lowering HGP. (nature.com)
  • Following the Pro-Resolution Nutrition system provides a clinically proven dietary program that helps reduce your levels of insulin resistance. (drsears.com)
  • This study will provide data that may serve as the basis for future studies on preventive strategies targeted at lowering insulin levels and increasing insulin sensitivity (e.g. decrease glucose, decrease abdominal fat, decrease omega-6 fatty acids/increase omega-3 fatty acids, increase fiber intake, increase exercise) in a subset of patients. (knowcancer.com)
  • A high intake of fructose (from added sugar , not fruit) has been linked to insulin resistance in both rats and humans ( 20 , 21 , 22 ). (healthline.com)
  • As I have reported here previously, Dr. Olefsky has been working to see how we can "block or disarm this macrophage inflammatory pathway in humans," preventing insulin resistance and type 2 diabetes. (mendosa.com)
  • Svetkey added, 'We also need to study the relationship between dietary intake of BCAA and insulin resistance in humans, and whether changing dietary patterns, beyond weight control, can improve matters. (medicalnewstoday.com)
  • Since animal studies proved the links of RBP4 and insulin resistance, researchers are keen to know about the same in humans. (medindia.net)
  • Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. (medscape.com)
  • SSPG, steady-state plasma glucose (determined by continuous infusion of somatostatin, insulin, and glucose during a 75-g oral glucose tolerance test). (diabetesjournals.org)
  • Plasma glucose and insulin concentrations were drawn every 10 min during the last 30 min of the infusion. (diabetesjournals.org)
  • Another study 4 published in 2013 found that type 2 diabetics given 50,000 IUs of oral vitamin D3 per week for eight weeks experienced "a meaningful reduction" in fasting plasma glucose and insulin. (mercola.com)
  • A steady-state plasma glucose test in individuals undergoing an insulin suppression test to assess insulin resistance found that the combination of insulin and C-peptide was a better indicator of insulin resistance than either one individually. (questdiagnostics.com)
  • The primary end point was changes in homeostasis model assessment of insulin resistance (HOMA-IR). (medscape.com)
  • Insulin resistance was derived from blood chemistry measures of fasting insulin and glucose using the homeostasis model assessment method. (diabetesjournals.org)
  • Insulin resistance was identified by the homeostasis model assessment for insulin resistance (HOMA-IR) index. (scielo.br)
  • Most actions of insulin are directed at metabolism (control) of carbohydrates (sugars and starches), lipids ( fats ), and proteins. (medicinenet.com)
  • the kinase activity autophosphorylates and mediates multiple actions of insulin. (medscape.com)
  • The above evidence suggests that actions of insulin may be involved in the promoting steps that predispose some women to breast cancer. (knowcancer.com)
  • [ 4 ] In the latter meta-analysis, pravastatin appeared to improve insulin sensitivity, whereas simvastatin was associated with an adverse effect on glucose metabolism. (medscape.com)
  • The WHO has similar criteria that include a prerequisite of diabetes, impaired glucose metabolism, or documented (by hyperinsulinemic-euglycemic clamp) insulin resistance. (jci.org)
  • Hepatic insulin resistance is sufficient to produce dyslipidemia and susceptibility to atherosclerosis," Cell Metabolism , vol. 7, no. 2, pp. 125-134, 2008. (hindawi.com)
  • The findings, in the November issue of Cell Metabolism, a Cell Press publication, suggest a new target for the treatment of insulin resistance and type 2 diabetes, the researchers say. (redorbit.com)
  • Although insulin is mostly implicated in blood sugar management, it also affects fat and protein metabolism. (healthline.com)
  • PPARγ-mediated gene regulation is the predominant mode of TZD-enhanced insulin sensitivity and metabolism. (pnas.org)
  • Dr. Barbara Kahn, chief of the division of diabetes, endocrinology and metabolism at Beth Israel Deaconess Medical Center, and a professor of medicine at Harvard Medical School in Boston finds that a substance closely bonded to insulin resistance and risk factors of heart disease. (medindia.net)
  • Patients with insulin resistance have problems with their glucose metabolism. (sparkpeople.com)
  • Research indicates that using a low GI (glycemic index) diet helps to reduce insulin insensitivity and improve glucose metabolism. (sparkpeople.com)
  • Foods that have independently been linked to insulin resistance include those high in sugar with high glycemic indices , high in dietary fat and fructose, low in omega-3 and fiber, and which are hyper-palatable which increases risk of overeating. (wikipedia.org)
  • Exercise activates the muscle cells that utilize blood sugar for energy and therefore increases insulin responsiveness. (news-medical.net)
  • Insulin also increases the uptake of fatty acids derived from circulating lipoproteins by stimulating lipoprotein lipase activity in adipose tissue. (jci.org)
  • Physical activity increases insulin sensitivity, and being inactive causes insulin resistance ( 25 , 26 ). (healthline.com)
  • Insulin resistance increases the chance of developing type 2 diabetes and heart disease. (scdhec.gov)
  • Will PCOS get better with a tummy tuck to reduce fat pad on belly that increases insulin r. (medhelp.org)
  • Weight loss typically lowers blood pressure and increases cell sensitivity to insulin. (sparkpeople.com)
  • Chromium supports insulin activity and increases the action of enzymes which digest sugars. (rainbow.coop)
  • Inflammation may play a role in insulin resistance, type 2 diabetes, and cardiovascular disease . (nih.gov)
  • Adipose tissue secretes various pro- and anti-inflammatory adipokines to modulate inflammation and insulin resistance. (springer.com)
  • Thus, we will describe the recent progress regarding the physiological and molecular function of adipokines in the obesity-induced inflammation and insulin resistance. (springer.com)
  • Chronic low-grade inflammation - common in adipose or fat tissue - is an important cause of systemic insulin resistance. (ucsd.edu)
  • Omega-3 fats reduce chronic inflammation and insulin resistance. (mendosa.com)
  • Chronic, low grade tissue inflammation is an important cause of obesity-related insulin resistance," the study states. (mendosa.com)
  • PITTSBURGH, Aug. 26 - An exploration of the molecular links between insulin resistance and inflammation may have revealed a novel target for diabetes treatment, say scientists at the John G. Rangos Sr. Research Center, Children's Hospital of Pittsburgh of UPMC. (eurekalert.org)
  • But it's not yet clear if there is a cause-and-effect relationship between chronic exposure to low-grade inflammation and the onset of insulin resistance," he explained. (eurekalert.org)
  • Other studies have shown that in patients who have inflammation and diabetes, insulin-sensitizing drugs seem to reduce inflammation while anti-inflammatory therapies improve sensitivity to insulin. (eurekalert.org)
  • Some researchers have theorized that the byproducts of oxidation may be responsible for inciting inflammation in fat cells, which in turn has been linked to insulin resistance and, ultimately, diabetes. (hopkinsmedicine.org)
  • Insulin resistance is one of the first consequences of unresolved inflammation. (drsears.com)
  • This is due to unresolved inflammation within the cell and why increased insulin resistance is also the first sign that chronic unresolved inflammation is increasing in your body. (drsears.com)
  • The higher your level of insulin resistance, the more likely you are to gain weight, develop chronic disease, and age faster as elevated insulin is driving force for increase inflammation. (drsears.com)
  • Using cross-sectional data from 766 fasting 12- to 19-year-olds in the 2003-2008 NHANES, we examined associations of phthalate metabolites with continuous and categorical measures of homeostatic model assessment of insulin resistance (HOMA-IR). (aappublications.org)
  • Associations persisted despite controlling for bisphenol A, another endocrine-disrupting chemical commonly found in foods, and HOMA-IR and insulin resistance were not significantly associated with metabolites of lower molecular weight phthalates commonly found in cosmetics and other personal care products. (aappublications.org)
  • Researchers compared PAD incidence and insulin sensitivity using a model of insulin resistance (HOMA-IR), a simple test derived from fasting glucose and insulin values. (emaxhealth.com)
  • Insulin resistance was assessed by homeostatic model assessment-estimated insulin resistance (HOMA-IR), insulin tolerance tests, and hyperinsulinemic-euglycemic clamps. (mdpi.com)
  • It is a non-insulin-based alternative to insulin-based methods to quantify peripheral insulin sensitivity and an alternative to the Homeostatic Model Assessment (HOMA-IR) and the quantitative insulin sensitivity check index (QUICKI). (wikipedia.org)
  • Cellular and tissue defects associated with insulin resistance are coincident with transcriptional abnormalities and are improved after insulin sensitization with thiazolidinedione (TZD) PPARγ ligands. (pnas.org)
  • Avandia and Actos, known generically as rosiglitazone and pioglitazone, are widely used to counteract the obesity-related abnormalities in insulin response that lead to diabetes. (scienceblog.com)
  • These are approved in the treatment of type 2 diabetes but not for the treatment of insulin resistance alone. (news-medical.net)
  • In addition, we also review the therapeutic strategies involving vitamin D in the treatment of insulin resistance. (scribd.com)
  • Cortisol counteracts insulin and can lead to increased hepatic gluconeogenesis , reduced peripheral utilization of glucose, and increased insulin resistance. (wikipedia.org)
  • Recently, inflammatory responses in adipose tissue have also been shown as one of the major mechanisms to induce peripheral tissue glucose intolerance and insulin resistance. (springer.com)
  • However, the molecular mechanisms underlying this crosstalk are still elusive, as well as how central and peripheral insulin signaling operate in AD ( Biessels and Despa, 2018 ). (frontiersin.org)
  • Researchers at Brigham and Women's Hospital (BWH) have shown for the first time that a strong association exists between insulin resistance and peripheral arterial disease (PAD), a risk factor for heart attacks and stroke. (emaxhealth.com)
  • We hypothesized that the lemon detox program would reduce body weight, body fat mass, thus lowering insulin resistance and known risk factors of cardiovascular disease. (nih.gov)
  • Therefore, we suppose that the lemon detox program reduces body fat and insulin resistance through caloric restriction and might have a potential beneficial effect on risk factors for cardiovascular disease related to circulating hs-CRP reduction without hematological changes. (nih.gov)
  • Association between insulin resistance and the development of cardiovascular disease. (webmd.com)
  • 2 ) showed that insulin resistance was a powerful independent predictor of a wide range of serious illnesses, including stroke, type 2 diabetes, cardiovascular disease, hypertension, and even cancer. (diabetesjournals.org)
  • Belly fat may also produce hormones and other substances that seem to instigate health issues like insulin resistance, high blood pressure, cholesterol imbalances and cardiovascular disease (CVD). (healthcentral.com)
  • 17 ] Because of the relationship between central adiposity and insulin resistance and because of the correlation between insulin resistance and increased cardiovascular disease risk, it has been suggested that health care providers should begin using waist measurements as a public health tool in screening for high-risk candidates for cardiovascular disease. (chiro.org)
  • Insulin resistance can lead to type 2 diabetes and can increase the risk for cardiovascular disease and stroke. (empowher.com)
  • This resistance occurs in response to the body's own insulin (endogenous) or when insulin is administered by injection (exogenous). (medicinenet.com)
  • Dog insulin resistance sometimes occurs in diabetic dogs. (vetinfo.com)
  • This is also known as the Somogyi response, and occurs when an excess amount of insulin is injected into the pet's body. (vetinfo.com)
  • Insulin resistance occurs when your cells become less responsive to the hormone. (livestrong.com)
  • Dr. Handelsman introduces himself and describes insulin resistance, a condition that occurs when the body does not properly use the insulin produced. (empowher.com)
  • To make things simple, insulin resistance occurs when the body has troubles utilizing insulin. (medical-supplies-equipment-company.com)
  • The signals downstream of PI3K are still unknown, and there is controversy as to whether the serine/threonine kinase Akt/protein kinase B (PKB) ( 6 , 7 ) or the protein kinase C (PKC) isoform λ/ζ ( 8 ) mediates insulin stimulation of glucose transport. (jci.org)
  • This study identifies monocyte chemoattractant protein 1 (MCP-1) as an insulin-responsive gene. (pnas.org)
  • Several studies have shown that decreased mitochondrial protein and oxidative phosphorylation (OXPHOS) in skeletal muscle and adipocytes are also underlying factors of insulin resistance ( 6 , 7 ). (pnas.org)
  • Kahn's group of researchers found 'RBP4, a protein that transports vitamin A in the blood may be a cause for insulin resistance' from animal studies. (medindia.net)
  • He wants to know if stopping the protein from working could help the body to use insulin and burn fat. (diabetes.org.uk)
  • Insulin is a chemical messenger that acts on the walls of the cells to cause the release, from within the cell, of special protein molecules - the so-called GLUT-4 transporters. (yourhealthbase.com)
  • The newly identified pathway linking obesity and insulin response involves cdk5, a protein kinase, or molecular "switch. (scienceblog.com)
  • 1 Association between insulin resistance and depression is a poorly studied area and the few earlier findings do not necessarily support this finding, 1 indicating that patients with serious depression have insulin resistance assessed by insulin tolerance, intravenous, or oral glucose tolerance tests. (bmj.com)
  • Recently, a novel association between insulin resistance and vitamin D deficiency has been proposed. (scribd.com)
  • Research is also supportive of the benefits of diets high in certain types of fiber for promoting improved post-prandial glucose and insulin responses in normal individuals and in individuals with type 2 diabetes, dyslipidemia, and insulin resistance. (chiro.org)
  • Because in our study higher depression scores were already prevalent in those with impaired glucose tolerance without clinically manifest diabetes, our findings might be explained biologically-that is, by pathophysiological changes behind insulin resistance and depression. (bmj.com)
  • Exposure to low-dose persistent organic pollutants appears to contribute to development of obesity, dyslipidemia, and insulin resistance. (greenmedinfo.com)
  • Therefore, it has been proposed that vitamin D deficiency plays an important role in insulin resistance resulting in diabetes. (scribd.com)
  • That is, the normal response to a given amount of insulin is reduced. (medicinenet.com)
  • The inventors describe methods for diagnosing or prognosing insulin resistance in diabetic and pre-diabetic patients, the method comprising determining the amount of insulin and C-peptide in a sample. (prlog.org)
  • Insulin is a hormone that allows glucose to enter cells which also reduces blood glucose (blood sugar). (wikipedia.org)
  • Insulin acts like a key to let blood sugar into cells for use as energy. (cdc.gov)
  • Insulin helps blood sugar enter the body's cells so it can be used for energy. (cdc.gov)
  • If you have insulin resistance, you want to become the opposite-more insulin sensitive (cells are more effective at absorbing blood sugar so less insulin is needed). (cdc.gov)
  • Insulin helps move the glucose (sugar) in your blood to parts of your body that need it to make energy, like the cells in your muscles. (webmd.com)
  • When you have insulin resistance, your cells aren't reacting to insulin the way they're supposed to -- they're resisting it -- and sugar stays in your blood. (webmd.com)
  • That's because there are many ways that insulin resistance affects your heart and blood vessels. (webmd.com)
  • The insulin produced is released into the blood stream and travels throughout the body. (medicinenet.com)
  • Insulin then lowers blood glucose to keep it in the normal range. (nih.gov)
  • Insulin given inappropriately can be a cause for elevated blood sugars. (vetinfo.com)
  • Bad insulin can also cause elevated blood sugars. (vetinfo.com)
  • If your diabetic dog suddenly requires a substantially higher dose of insulin to keep his blood sugars in line, it's important to consult your veterinarian. (vetinfo.com)
  • Most pets are prescribed long acting insulin medication that controls blood glucose for a longer period of time. (vetinfo.com)
  • Pets suffering from insulin resistance may have a high number of antibodies present in the blood. (vetinfo.com)
  • In insulin resistance, cells and muscles stop absorbing glucose as efficiently and more glucose stays in the blood," explained Rebecca Elbaum, RD, CDE. (popsugar.com)
  • Eventually, the cells that secrete insulin fail to keep up with the body's need and blood glucose builds up in the blood stream and stays elevated. (popsugar.com)
  • This type of fat may release lots of free fatty acids into the blood, and can even release inflammatory hormones that drive insulin resistance ( 16 , 17 , 18 ). (healthline.com)
  • Most medications and insulin therapy are aimed at lowering blood sugar through increasing insulin. (huffingtonpost.com)
  • A balanced blood sugar level can help reduce the risk of insulin resistance. (livestrong.com)
  • As obesity and diabetes rates continue to rise, research into the role of insulin resistance and how different types of sugar influence blood glucose balance is gaining prominence. (livestrong.com)
  • As reported in this issue of Circulation , Ärnlöv and colleagues 6 investigated the relationship between insulin sensitivity, using ISI, and the 4-year incidence of hypertension and blood pressure (BP) progression in 1933 nonhypertensive participants in the Framingham Offspring Study. (ahajournals.org)
  • Under normal conditions of insulin reactivity, this insulin response triggers glucose being taken into body cells, to be used for energy , and inhibits the body from using fat for energy, thereby causing the concentration of glucose in the blood to decrease as a result, staying within the normal range even when a large amount of carbohydrates is consumed. (wikipedia.org)
  • Researchers at the University of California, San Diego School of Medicine say neutrophils, an abundant type of white blood cell typically tasked with attacking bacteria and other foreign invaders, also plays an unexpected role in mediating insulin resistance - the central characteristic of type 2 diabetes, which afflicts an estimated 26 million Americans. (ucsd.edu)
  • The general hypothesis is that cognitive and vascular function is impaired via shift away from insulin-mediated vasodilation in brain blood vessels. (bioportfolio.com)
  • Insulin helps cells grab glucose from the blood. (scienceblog.com)
  • After a year on pioglitazone, these women also had a greater reduction in insulin in the blood-a marker of a reduced load on their beta cells. (scienceblog.com)
  • Insulin is a natural hormone that controls our blood sugar. (medindia.net)
  • Lower glycemic foods will usually cause less insulin to be released, and probably will allow blood sugar to be better regulated. (empowher.com)
  • Washington D.C. [USA], Mar. 23 : Higher level of blood sugar and insulin resistance, accompanied by obesity and physical inactivity, is also linked to more rapid decline in cognitive performance, says a new study. (topnews.in)
  • Insulin resistance is when your body doesn't respond properly to the insulin that you produce, so glucose can't move from your blood into your cells. (diabetes.org.uk)
  • Monitor your blood glucose, insulin, mood, HbA1c and lots more with the only diabetes app. (diabetes.co.uk)
  • Physical activity makes you more sensitive to insulin, one reason why it's a cornerstone of diabetes management (and good health in general! (cdc.gov)
  • Insulin resistance makes cells less sensitive to insulin. (medicalnewstoday.com)
  • If you do start to exercise, the muscles become more sensitive to insulin and glucose uptake and utilization of available sugar is improved. (healthcentral.com)
  • PAI-1 and SREBP-1c ) that remain sensitive to insulin in IR states. (pnas.org)
  • Pioglitazone makes the body's cells more sensitive to insulin, reducing beta cells' workload. (scienceblog.com)
  • Insulin promotes adipocyte triglyceride stores by a number of mechanisms, including fostering the differentiation of preadipocytes to adipocytes and, in mature adipocytes, stimulating glucose transport and triglyceride synthesis (lipogenesis), as well as inhibiting lipolysis (Figure 1 ). (jci.org)
  • Actually, quite a lot is known about the mechanisms of insulin resistance. (diabetesdaily.com)
  • This study shows that our initial findings for diabetes prevention with troglitazone apply not only to this class of drugs-thiazolidinediones-but to the general mechanisms of reducing stress on beta cells by treating insulin resistance," Buchanan says. (scienceblog.com)
  • The team is currently studying the vascular and non-vascular mechanisms by which insulin resistance may affect cognition. (topnews.in)
  • Possible Mechanisms linking Ageing, Obesity, Sarcopenia and Insulin resistance (Zamboni et al. (intechopen.com)
  • There are several reasons why a dog might develop insulin resistance. (vetinfo.com)
  • A diabetic dog can also develop insulin resistance due to the presence of other diseases. (vetinfo.com)
  • Certain drugs can cause a diabetic dog to develop insulin resistance. (vetinfo.com)
  • Scientists have identified specific genes that make people more likely to develop insulin resistance and diabetes. (scdhec.gov)
  • Exercise may help prevent insulin resistance. (medicinenet.com)
  • Exercising, maintaining a balanced and healthy diet, and watching your weight will help you prevent insulin resistance and, as a result, protect your brain as you get older. (topnews.in)
  • There are a few things you can do that can help prevent insulin resistance. (medmovie.com)
  • Contrary to expectations, preventing the burning of fats within fat cells does not prevent insulin resistance, a mouse study finds. (hopkinsmedicine.org)
  • A mismatch between the circadian rhythm and the meals schedule, such as in circadian rhythm disorders , may increase insulin resistance. (wikipedia.org)
  • Testosterone suppression and/or low testosterone may increase insulin resistance in men. (greenmedinfo.com)
  • These effects of vitamin D deficiency, either acting in concert or alone, all serve to increase insulin resistance. (scribd.com)
  • Weight gain can also cause insulin resistance. (vetinfo.com)
  • In addition, insulin that has passed the expiration date or insulin that's kept in high temperatures may not function effectively, and can cause insulin resistance. (vetinfo.com)
  • The results of a study, reported in Gastroenterology (March 2004), indicate that hepatitis C virus (HCV) infection can directly cause insulin resistance. (pharmacytimes.com)
  • [9] This acute form of insulin resistance that may result post-operatively tends to increase over the short term, with sensitivity to insulin typically returning to patients after about five days. (wikipedia.org)
  • Improving your body's sensitivity to insulin can help curb hunger, stabilize weight and improve cardiovascular health and fasting may just be the way to do that. (healthstatus.com)
  • Studies have shown that significantly reducing calorific intake can improve the body's sensitivity to insulin. (diabetes.co.uk)
  • Loss of insulin signaling in hepatocytes leads to severe insulin resistance and progressive hepatic dysfunction," Molecular Cell , vol. 6, no. 1, pp. 87-97, 2000. (hindawi.com)
  • Phosphoenolpyruvate carboxykinase overexpression selectively attenuates insulin signaling and hepatic insulin sensitivity in transgenic mice," The Journal of Biological Chemistry , vol. 277, no. 26, pp. 23301-23307, 2002. (hindawi.com)
  • Furthermore, the increase in hepatic insulin sensitivity observed in patients with type 2 diabetes following weight loss is also accompanied by a significant reduction in intrahepatic fat without any changes in circulating adipocytokines (interleukin-6, resistin, leptin). (nih.gov)
  • Further, we found that duodenum-specific knockdown of Sirt1 expression for 14 d was sufficient to induce hepatic insulin resistance in rats fed normal chow. (nature.com)
  • High-fat diet-mediated lipotoxicity and insulin resistance is related to impaired lipase expression in mouse skeletal muscle. (springer.com)
  • Novel investigational techniques based on magnetic resonance spectroscopy (MRS) have allowed real-time insight into the molecular defects in patients with type 2 diabetes, revealing that insulin resistance is a product of decreased insulin-stimulated skeletal muscle glycogen synthesis, which can mostly be attributed to decreased insulin-stimulated glucose transport (Glut 4) activity. (nih.gov)
  • From a quantitative standpoint, skeletal muscle is presumed to have the greatest impact on whole-body glucose disposal, and hence on insulin resistance. (chiro.org)