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InsulinReceptor, InsulinInsulin ResistanceInsulin Receptor Substrate ProteinsGlucoseInsulin, Long-ActingInsulin AntibodiesHypoglycemic AgentsInsulin AntagonistsIslets of LangerhansInsulin LisproGlucose Tolerance TestDiabetes Mellitus, Type 2Insulin Infusion SystemsGlucose Clamp TechniqueInsulin AspartInsulin, IsophaneInsulin, Regular, PorkHyperinsulinismAdipose TissueInsulin-Secreting CellsInsulinsGlucagonObesityInsulin, Regular, HumanC-PeptideProinsulinFastingBlood GlucoseHyperglycemiaLiverMuscle, SkeletalDiabetes Mellitus, Type 1Signal TransductionFatty Acids, NonesterifiedGlucose Transporter Type 4AdipocytesInsulin, Short-ActingHypoglycemiaPhosphorylationDiabetes Mellitus, ExperimentalDiabetes MellitusGlucose IntoleranceInsulin-Like Growth Factor ILeptinDeoxyglucoseBody WeightTriglyceridesPhosphoproteinsMonosaccharide Transport ProteinsPhosphatidylinositol 3-KinasesInsulinomaCells, CulturedBiphasic InsulinsKineticsProto-Oncogene Proteins c-aktHemoglobin A, GlycosylatedGlycogenHomeostasisAdiponectinPostprandial PeriodRats, WistarLipidsTime FactorsPancreasGlucagon-Like Peptide 1Cell LineBody Mass IndexMetforminDietary FatsDose-Response Relationship, DrugMice, ObeseLipid MetabolismRNA, MessengerRats, Inbred StrainsThiazolidinediones3T3-L1 CellsLipolysisMuscle ProteinsRats, Sprague-DawleyReceptor, IGF Type 1Rats, ZuckerMice, Inbred C57BLMetabolic Syndrome XTolbutamideInfusions, SubcutaneousEatingDietary CarbohydratesGene Expression RegulationBody CompositionBiological TransportDiet, High-FatReference ValuesStreptozocinMice, KnockoutEnergy MetabolismGlycogen SynthaseSomatostatinAdiposityGluconeogenesis3-O-MethylglucoseGlucokinaseEnzyme ActivationGrowth HormoneFatty LiverTyrosineInjections, SubcutaneousPolycystic Ovary Syndrome3T3 CellsFatty AcidsProtein-Serine-Threonine KinasesHormonesInsulysinSulfonylurea CompoundsFructoseCell MembraneGastric Inhibitory PolypeptideModels, BiologicalDiabetic KetoacidosisPrediabetic StateProteinsMusclesCricetinaeDietProtein Tyrosine Phosphatase, Non-Receptor Type 1Glucose Transporter Type 2Cross-Over StudiesInfusions, IntravenousMolecular Sequence DataAndrostadienesProtein-Tyrosine KinasesRibosomal Protein S6 KinasesDiazoxideBlotting, WesternEpinephrineGlycerolResistinIntra-Abdominal FatGene ExpressionMethylglucosidesRisk FactorsLeucinePregnancyAdipokinesTransfectionAmino AcidsStimulation, ChemicalVenomsPalmitatesBlood PressureCalciumEnzyme InhibitorsExocytosisReceptors, SomatomedinDisease Models, AnimalBiological MarkersMice, TransgenicCHO CellsAmino Acid SequenceArea Under CurveHydrocortisoneIntracellular Signaling Peptides and ProteinsIslets of Langerhans TransplantationBlood Glucose Self-MonitoringEnergy IntakeGhrelinWeight GainGlucose Transporter Type 1Adenoma, Islet CellPhosphotyrosineOxidation-ReductionPPAR gammaPalmitic AcidDexamethasoneProto-Oncogene ProteinsInsulin ComaPancreas, ArtificialDiabetes, GestationalTranscription FactorsReverse Transcriptase Polymerase Chain ReactionInsulin-Like Growth Factor IICyclic AMPRadioimmunoassayAnalysis of VarianceSwineLactatesGlucose-6-PhosphataseArginineAgingReceptors, GlucagonWeight Loss3-Hydroxybutyric AcidPerfusionSecretory RateLactic AcidInflammationAdipose Tissue, WhiteAdenosine TriphosphateGlycolysisProtein KinasesRecombinant Proteins
Insulin: 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).Receptor, Insulin: 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.Insulin Resistance: 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.Insulin Receptor Substrate Proteins: 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.Glucose: 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.Insulin, Long-Acting: Insulin formulations that contain substances that retard absorption thus extending the time period of action.Insulin Antibodies: Antibodies specific to INSULIN.Hypoglycemic Agents: Substances which lower blood glucose levels.Insulin Antagonists: Compounds which inhibit or antagonize the biosynthesis or action of insulin.Islets of Langerhans: 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.Insulin Lispro: 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.Glucose Tolerance Test: 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).Diabetes Mellitus, Type 2: 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.Insulin Infusion Systems: 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.Glucose Clamp Technique: 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.Insulin Aspart: Insulin that has been modified to contain an ASPARTIC ACID instead of a PROLINE at position 38 of the B-chain.Insulin, Isophane: 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.Insulin, Regular, Pork: Regular insulin preparations that contain the SUS SCROFA insulin peptide sequence.Hyperinsulinism: 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.Adipose Tissue: 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.Insulin-Secreting Cells: A type of pancreatic cell representing about 50-80% of the islet cells. Beta cells secrete INSULIN.Insulins: 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.Glucagon: 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)Obesity: 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).Insulin, Regular, Human: Regular insulin preparations that contain the HUMAN insulin peptide sequence.C-Peptide: 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.Proinsulin: 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.Fasting: Abstaining from all food.Blood Glucose: Glucose in blood.Hyperglycemia: Abnormally high BLOOD GLUCOSE level.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Muscle, Skeletal: 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.Diabetes Mellitus, Type 1: 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.Signal Transduction: 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.Fatty Acids, Nonesterified: FATTY ACIDS found in the plasma that are complexed with SERUM ALBUMIN for transport. These fatty acids are not in glycerol ester form.Glucose Transporter Type 4: 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.Adipocytes: 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.Insulin, Short-Acting: Insulin derivatives and preparations that are designed to induce a rapid HYPOGLYCEMIC EFFECT.Hypoglycemia: 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.Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.Diabetes Mellitus, Experimental: Diabetes mellitus induced experimentally by administration of various diabetogenic agents or by PANCREATECTOMY.Diabetes Mellitus: A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.Glucose Intolerance: 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.Insulin-Like Growth Factor I: 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.Leptin: 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.Deoxyglucose: 2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.Body Weight: The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.TriglyceridesPhosphoproteinsMonosaccharide Transport Proteins: A large group of membrane transport proteins that shuttle MONOSACCHARIDES across CELL MEMBRANES.Phosphatidylinositol 3-Kinases: 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.Insulinoma: A benign tumor of the PANCREATIC BETA CELLS. Insulinoma secretes excess INSULIN resulting in HYPOGLYCEMIA.Cells, Cultured: 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.Biphasic Insulins: An insulin preparation that is designed to provide immediate and long term glycemic control in a single dosage. Biphasic insulin typically contains a mixture of REGULAR INSULIN or SHORT-ACTING INSULIN combined with a LONG-ACTING INSULIN.Kinetics: The rate dynamics in chemical or physical systems.Proto-Oncogene Proteins c-akt: 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.Hemoglobin A, Glycosylated: 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.GlycogenHomeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable.Adiponectin: 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.Postprandial Period: The time frame after a meal or FOOD INTAKE.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Lipids: 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)Time Factors: Elements of limited time intervals, contributing to particular results or situations.Pancreas: 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.Glucagon-Like Peptide 1: 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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Body Mass Index: 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)Metformin: 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)Dietary Fats: 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.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Mice, Obese: 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.Lipid Metabolism: Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.RNA, Messenger: 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.Rats, Inbred Strains: Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.Thiazolidinediones: 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).3T3-L1 Cells: 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.Lipolysis: 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.Muscle Proteins: The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.Rats, Sprague-Dawley: 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.Receptor, IGF Type 1: A protein-tyrosine kinase receptor that is closely related in structure to the INSULIN RECEPTOR. Although commonly referred to as the IGF-I receptor, it binds both IGF-I and IGF-II with high affinity. It is comprised of a tetramer of two alpha and two beta subunits which are derived from cleavage of a single precursor protein. The beta subunit contains an intrinsic tyrosine kinase domain.Rats, Zucker: 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.Mice, Inbred C57BLMetabolic Syndrome X: 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)Tolbutamide: A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290)Infusions, Subcutaneous: The administration of liquid medication or nutrients under the skin, usually over minutes or hours.Eating: The consumption of edible substances.Dietary Carbohydrates: 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)Gene Expression Regulation: 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.Body Composition: The relative amounts of various components in the body, such as percentage of body fat.Biological Transport: 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.Diet, High-Fat: Consumption of excessive DIETARY FATS.Reference Values: 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.Streptozocin: An antibiotic that is produced by Stretomyces achromogenes. It is used as an antineoplastic agent and to induce diabetes in experimental animals.Mice, Knockout: 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.Energy Metabolism: The chemical reactions involved in the production and utilization of various forms of energy in cells.Glycogen Synthase: An enzyme that catalyzes the transfer of D-glucose from UDPglucose into 1,4-alpha-D-glucosyl chains. EC 2.4.1.11.Somatostatin: A 14-amino acid peptide named for its ability to inhibit pituitary GROWTH HORMONE release, also called somatotropin release-inhibiting factor. It is expressed in the central and peripheral nervous systems, the gut, and other organs. SRIF can also inhibit the release of THYROID-STIMULATING HORMONE; PROLACTIN; INSULIN; and GLUCAGON besides acting as a neurotransmitter and neuromodulator. In a number of species including humans, there is an additional form of somatostatin, SRIF-28 with a 14-amino acid extension at the N-terminal.Adiposity: The amount of fat or lipid deposit at a site or an organ in the body, an indicator of body fat status.Gluconeogenesis: Biosynthesis of GLUCOSE from nonhexose or non-carbohydrate precursors, such as LACTATE; PYRUVATE; ALANINE; and GLYCEROL.3-O-Methylglucose: A non-metabolizable glucose analogue that is not phosphorylated by hexokinase. 3-O-Methylglucose is used as a marker to assess glucose transport by evaluating its uptake within various cells and organ systems. (J Neurochem 1993;60(4):1498-504)Glucokinase: A group of enzymes that catalyzes the conversion of ATP and D-glucose to ADP and D-glucose 6-phosphate. They are found in invertebrates and microorganisms, and are highly specific for glucose. (Enzyme Nomenclature, 1992) EC 2.7.1.2.Enzyme Activation: 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.Growth Hormone: A polypeptide that is secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). Growth hormone, also known as somatotropin, stimulates mitosis, cell differentiation and cell growth. Species-specific growth hormones have been synthesized.Fatty Liver: 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.Tyrosine: A non-essential amino acid. In animals it is synthesized from PHENYLALANINE. It is also the precursor of EPINEPHRINE; THYROID HORMONES; and melanin.Injections, Subcutaneous: Forceful administration under the skin of liquid medication, nutrient, or other fluid through a hollow needle piercing the skin.Polycystic Ovary Syndrome: 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.3T3 Cells: Cell lines whose original growing procedure consisted being transferred (T) every 3 days and plated at 300,000 cells per plate (J Cell Biol 17:299-313, 1963). Lines have been developed using several different strains of mice. Tissues are usually fibroblasts derived from mouse embryos but other types and sources have been developed as well. The 3T3 lines are valuable in vitro host systems for oncogenic virus transformation studies, since 3T3 cells possess a high sensitivity to CONTACT INHIBITION.Fatty Acids: 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)Protein-Serine-Threonine Kinases: A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.Hormones: Chemical substances having a specific regulatory effect on the activity of a certain organ or organs. The term was originally applied to substances secreted by various ENDOCRINE GLANDS and transported in the bloodstream to the target organs. It is sometimes extended to include those substances that are not produced by the endocrine glands but that have similar effects.Insulysin: An enzyme the catalyzes the degradation of insulin, glucagon and other polypeptides. It is inhibited by bacitracin, chelating agents EDTA and 1,10-phenanthroline, and by thiol-blocking reagents such as N-ethylmaleimide, but not phosphoramidon. (Eur J Biochem 1994;223:1-5) EC 3.4.24.56.Sulfonylurea CompoundsFructose: 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.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Gastric Inhibitory Polypeptide: A gastrointestinal peptide hormone of about 43-amino acids. It is found to be a potent stimulator of INSULIN secretion and a relatively poor inhibitor of GASTRIC ACID secretion.Models, Biological: 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.Diabetic Ketoacidosis: A life-threatening complication of diabetes mellitus, primarily of TYPE 1 DIABETES MELLITUS with severe INSULIN deficiency and extreme HYPERGLYCEMIA. It is characterized by KETOSIS; DEHYDRATION; and depressed consciousness leading to COMA.Prediabetic State: 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).Proteins: 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.Muscles: Contractile tissue that produces movement in animals.Cricetinae: A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.Diet: Regular course of eating and drinking adopted by a person or animal.Protein Tyrosine Phosphatase, Non-Receptor Type 1: 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.Glucose Transporter Type 2: A glucose transport facilitator that is expressed primarily in PANCREATIC BETA CELLS; LIVER; and KIDNEYS. It may function as a GLUCOSE sensor to regulate INSULIN release and glucose HOMEOSTASIS.Cross-Over Studies: Studies comparing two or more treatments or interventions in which the subjects or patients, upon completion of the course of one treatment, are switched to another. In the case of two treatments, A and B, half the subjects are randomly allocated to receive these in the order A, B and half to receive them in the order B, A. A criticism of this design is that effects of the first treatment may carry over into the period when the second is given. (Last, A Dictionary of Epidemiology, 2d ed)Infusions, Intravenous: The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.Molecular Sequence Data: 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.Androstadienes: Derivatives of the steroid androstane having two double bonds at any site in any of the rings.Protein-Tyrosine Kinases: Protein kinases that catalyze the PHOSPHORYLATION of TYROSINE residues in proteins with ATP or other nucleotides as phosphate donors.Ribosomal Protein S6 Kinases: A family of protein serine/threonine kinases which act as intracellular signalling intermediates. Ribosomal protein S6 kinases are activated through phosphorylation in response to a variety of HORMONES and INTERCELLULAR SIGNALING PEPTIDES AND PROTEINS. Phosphorylation of RIBOSOMAL PROTEIN S6 by enzymes in this class results in increased expression of 5' top MRNAs. Although specific for RIBOSOMAL PROTEIN S6 members of this class of kinases can act on a number of substrates within the cell. The immunosuppressant SIROLIMUS inhibits the activation of ribosomal protein S6 kinases.Diazoxide: A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group.Blotting, Western: 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.Epinephrine: The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent.Resistin: 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.Intra-Abdominal Fat: 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.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.MethylglucosidesRisk Factors: 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.Leucine: An essential branched-chain amino acid important for hemoglobin formation.Pregnancy: The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.Adipokines: 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.Transfection: The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (-COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins.Stimulation, Chemical: The increase in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.Venoms: Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling prey or predator.Palmitates: Salts and esters of the 16-carbon saturated monocarboxylic acid--palmitic acid.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Exocytosis: Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the CELL MEMBRANE.Receptors, Somatomedin: Cell surface receptors that bind somatomedins and trigger intracellular changes which influence the behavior of cells. Studies have disclosed two types of receptors for this family of peptide hormones. The type I receptor is homologous to the insulin receptor and has tyrosine kinase activity. The type II receptor is identical to the mannose-6-phosphate receptor which is important in trafficking of lysosomal enzymes.Disease Models, Animal: 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.Biological Markers: 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.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.CHO Cells: CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.Amino Acid Sequence: 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.Area Under Curve: A statistical means of summarizing information from a series of measurements on one individual. It is frequently used in clinical pharmacology where the AUC from serum levels can be interpreted as the total uptake of whatever has been administered. As a plot of the concentration of a drug against time, after a single dose of medicine, producing a standard shape curve, it is a means of comparing the bioavailability of the same drug made by different companies. (From Winslade, Dictionary of Clinical Research, 1992)Hydrocortisone: The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.Intracellular Signaling Peptides and Proteins: Proteins and peptides that are involved in SIGNAL TRANSDUCTION within the cell. Included here are peptides and proteins that regulate the activity of TRANSCRIPTION FACTORS and cellular processes in response to signals from CELL SURFACE RECEPTORS. Intracellular signaling peptide and proteins may be part of an enzymatic signaling cascade or act through binding to and modifying the action of other signaling factors.Islets of Langerhans Transplantation: The transference of pancreatic islets within an individual, between individuals of the same species, or between individuals of different species.Blood Glucose Self-Monitoring: Self evaluation of whole blood glucose levels outside the clinical laboratory. A digital or battery-operated reflectance meter may be used. It has wide application in controlling unstable insulin-dependent diabetes.Energy Intake: Total number of calories taken in daily whether ingested or by parenteral routes.Ghrelin: A 28-amino acid, acylated, orexigenic peptide that is a ligand for GROWTH HORMONE SECRETAGOGUE RECEPTORS. Ghrelin is widely expressed but primarily in the stomach in the adults. Ghrelin acts centrally to stimulate growth hormone secretion and food intake, and peripherally to regulate energy homeostasis. Its large precursor protein, known as appetite-regulating hormone or motilin-related peptide, contains ghrelin and obestatin.Weight Gain: Increase in BODY WEIGHT over existing weight.Glucose Transporter Type 1: A ubiquitously expressed glucose transporter that is important for constitutive, basal GLUCOSE transport. It is predominately expressed in ENDOTHELIAL CELLS and ERYTHROCYTES at the BLOOD-BRAIN BARRIER and is responsible for GLUCOSE entry into the BRAIN.Adenoma, Islet Cell: A benign tumor of the pancreatic ISLET CELLS. Usually it involves the INSULIN-producing PANCREATIC BETA CELLS, as in INSULINOMA, resulting in HYPERINSULINISM.Phosphotyrosine: An amino acid that occurs in endogenous proteins. Tyrosine phosphorylation and dephosphorylation plays a role in cellular signal transduction and possibly in cell growth control and carcinogenesis.Oxidation-Reduction: 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).PPAR gamma: 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.Palmitic Acid: A common saturated fatty acid found in fats and waxes including olive oil, palm oil, and body lipids.Dexamethasone: An anti-inflammatory 9-fluoro-glucocorticoid.Proto-Oncogene Proteins: Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.Insulin Coma: Severe HYPOGLYCEMIA induced by a large dose of exogenous INSULIN resulting in a COMA or profound state of unconsciousness from which the individual cannot be aroused.Pancreas, Artificial: Devices for simulating the activity of the pancreas. They can be either electromechanical, consisting of a glucose sensor, computer, and insulin pump or bioartificial, consisting of isolated islets of Langerhans in an artificial membrane.Diabetes, Gestational: 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.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Reverse Transcriptase Polymerase Chain Reaction: 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.Insulin-Like Growth Factor II: A well-characterized neutral peptide believed to be secreted by the LIVER and to circulate in the BLOOD. It has growth-regulating, insulin-like and mitogenic activities. The growth factor has a major, but not absolute, dependence on SOMATOTROPIN. It is believed to be a major fetal growth factor in contrast to INSULIN-LIKE GROWTH FACTOR I, which is a major growth factor in adults.Cyclic AMP: An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.Radioimmunoassay: Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation.Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.Swine: Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).Lactates: Salts or esters of LACTIC ACID containing the general formula CH3CHOHCOOR.Glucose-6-Phosphatase: An enzyme that catalyzes the conversion of D-glucose 6-phosphate and water to D-glucose and orthophosphate. EC 3.1.3.9.Arginine: An essential amino acid that is physiologically active in the L-form.Aging: The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.Receptors, Glucagon: Cell surface receptors that bind glucagon with high affinity and trigger intracellular changes which influence the behavior of cells. Activation of glucagon receptors causes a variety of effects; the best understood is the initiation of a complex enzymatic cascade in the liver which ultimately increases the availability of glucose to body organs.Weight Loss: Decrease in existing BODY WEIGHT.3-Hydroxybutyric Acid: BUTYRIC ACID substituted in the beta or 3 position. It is one of the ketone bodies produced in the liver.Perfusion: Treatment process involving the injection of fluid into an organ or tissue.Secretory Rate: The amount of a substance secreted by cells or by a specific organ or organism over a given period of time; usually applies to those substances which are formed by glandular tissues and are released by them into biological fluids, e.g., secretory rate of corticosteroids by the adrenal cortex, secretory rate of gastric acid by the gastric mucosa.Lactic Acid: A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed)Inflammation: 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.Adipose Tissue, White: 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.Adenosine Triphosphate: An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.Glycolysis: A metabolic process that converts GLUCOSE into two molecules of PYRUVIC ACID through a series of enzymatic reactions. Energy generated by this process is conserved in two molecules of ATP. Glycolysis is the universal catabolic pathway for glucose, free glucose, or glucose derived from complex CARBOHYDRATES, such as GLYCOGEN and STARCH.Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein.Recombinant Proteins: Proteins prepared by recombinant DNA technology.

Effect of trauma on plasma glucagon and insulin concentrations in sheep. (1/30793)

Portal plasma glucagon and insulin concentrations were measured before and after acute trauma (liver biosy). The trauma was sufficient to increase glucagon concentrations and depress insulin concentrations. These changes were associated with a marked hyperglycemia. Infusion of glucagon was insufficient to prevent stress inhibition of insulin secretion. The stimulation of glucagon secretion and inhibition of insulin secretion were of about one hour duration. These findings indicate that glucagon and insulin in conjunction with the nervous system may play an important role in the development of stress related hyperglycemia.  (+info)

Effects of glucagon and insulin on lipolysis and ketogenesis in sheep. (2/30793)

The hepatic and portal productions of acetoacetate and beta-hydroxybutyrate and lipolysis were studied in normal and insulin-controlled alloxan-diabetic sheep. Since hyperinsulinemia is associated with glucagon administration, the latter group of sheep were used to maintain constant plasma insulin levels. After control values were obtained glucagon was infused intraportally at 90 mug/hr for two hours. The ketone body production by portal drained viscera was not significantly affected by glucagon. In alloxanized sheep, glucagon significantly (P less than 0.01) increased net hepatic production of acetoacetate (from -0.54 +/- 0.08 to 0.46 +/- 0.07 g/hr). Lipolysis also increased. However, in the normal sheep, hyperinsulinemia prevented any stimulatory effect of glucagon on hepatic ketogenesis and lipolysis. Therefore, while glucagon appears capable of stimulating ketogenesis andlipolysis, these effects are readily suppressed by insulin.  (+info)

Vasopressin stimulation of acetate incorporation into lipids in a dimethylbenz(a)anthracene-induced rat mammary tumor cell line. (3/30793)

In a preliminary report we described the effects of rat prolactin on the incorporation of [14C]acetate into lipids by a cell line from a dimethylbenz(a)anthracene-induced rat mammary tumor. The characteristics of the response to prolactin were very similar to those described for the normal rat mammary gland; namely, insulin was required for full expression of the response, maximal activity was not seen until 36 hr after the addition of the hormones, and growth hormone was able to elicit the same response. However, we were unable to detect binding of 125I-labeled prolactin to these cells, and furthermore, other more purified prolactin preparations were inactive. Upon further investigation we discovered that the activity resided in a low-molecular-weight fraction of the rat prolactin B-1 preparation and was probably either vasopressin or oxytocin or both. These data suggest the possibility that vasopressin may play a role in rodent mammary tumorigenesis.  (+info)

Leptin suppression of insulin secretion and gene expression in human pancreatic islets: implications for the development of adipogenic diabetes mellitus. (4/30793)

Previously we demonstrated the expression of the long form of the leptin receptor in rodent pancreatic beta-cells and an inhibition of insulin secretion by leptin via activation of ATP-sensitive potassium channels. Here we examine pancreatic islets isolated from pancreata of human donors for their responses to leptin. The presence of leptin receptors on islet beta-cells was demonstrated by double fluorescence confocal microscopy after binding of a fluorescent derivative of human leptin (Cy3-leptin). Leptin (6.25 nM) suppressed insulin secretion of normal islets by 20% at 5.6 mM glucose. Intracellular calcium responses to 16.7 mM glucose were rapidly reduced by leptin. Proinsulin messenger ribonucleic acid expression in islets was inhibited by leptin at 11.1 mM, but not at 5.6 mM glucose. Leptin also reduced proinsulin messenger ribonucleic acid levels that were increased in islets by treatment with 10 nM glucagon-like peptide-1 in the presence of either 5.6 or 11.1 mM glucose. These findings demonstrate direct suppressive effects of leptin on insulin-producing beta-cells in human islets at the levels of both stimulus-secretion coupling and gene expression. The findings also further indicate the existence of an adipoinsular axis in humans in which insulin stimulates leptin production in adipocytes and leptin inhibits the production of insulin in beta-cells. We suggest that dysregulation of the adipoinsular axis in obese individuals due to defective leptin reception by beta-cells may result in chronic hyperinsulinemia and may contribute to the pathogenesis of adipogenic diabetes.  (+info)

Cardiovascular disease in insulin dependent diabetes mellitus: similar rates but different risk factors in the US compared with Europe. (5/30793)

BACKGROUND: Cardiovascular disease (CVD) in insulin dependent diabetes mellitus (IDDM) has been linked to renal disease. However, little is known concerning international variation in the correlations with hyperglycaemia and standard CVD risk factors. METHODS: A cross-sectional comparison was made of prevalence rates and risk factor associations in two large studies of IDDM subjects: the Pittsburgh Epidemiology of Diabetes Complications Study (EDC) and the EURODIAB IDDM Complications Study from 31 centres in Europe. Subgroups of each were chosen to be comparable by age and duration of diabetes. The EDC population comprises 286 men (mean duration 20.1 years) and 281 women (mean duration 19.9 years); EURODIAB 608 men (mean duration 18.1 years) and 607 women (mean duration 18.9 years). The mean age of both populations was 28 years. Cardiovascular disease was defined by a past medical history of myocardial infarction, angina, and/or the Minnesota ECG codes (1.1-1.3, 4.1-4.3, 5.1-5.3, 7.1). RESULTS: Overall prevalence of CVD was similar in the two populations (i.e. men 8.6% versus 8.0%, women 7.4% versus 8.5%, EURODIAB versus EDC respectively), although EDC women had a higher prevalence of angina (3.9% versus 0.5%, P < 0.001). Multivariate modelling suggests that glycaemic control (HbA1c) is not related to CVD in men. Age and high density lipoprotein cholesterol predict CVD in EURODIAB, while triglycerides and hypertension predict CVD in EDC. For women in both populations, age and hypertension (or renal disease) are independent predictors. HbA1c is also an independent predictor-inversely in EURODIAB women (P < 0.008) and positively in EDC women (P = 0.03). Renal disease was more strongly linked to CVD in EDC than in EURODIAB. CONCLUSIONS: Despite a similar prevalence of CVD, risk factor associations appear to differ in the two study populations. Glycaemic control (HbA1c) does not show a consistent or strong relationship to CVD.  (+info)

Tissue-specific knockout of the insulin receptor in pancreatic beta cells creates an insulin secretory defect similar to that in type 2 diabetes. (6/30793)

Dysfunction of the pancreatic beta cell is an important defect in the pathogenesis of type 2 diabetes, although its exact relationship to the insulin resistance is unclear. To determine whether insulin signaling has a functional role in the beta cell we have used the Cre-loxP system to specifically inactivate the insulin receptor gene in the beta cells. The resultant mice exhibit a selective loss of insulin secretion in response to glucose and a progressive impairment of glucose tolerance. These data indicate an important functional role for the insulin receptor in glucose sensing by the pancreatic beta cell and suggest that defects in insulin signaling at the level of the beta cell may contribute to the observed alterations in insulin secretion in type 2 diabetes.  (+info)

Hormonal regulation of messenger ribonucleic acid expression for steroidogenic factor-1, steroidogenic acute regulatory protein, and cytochrome P450 side-chain cleavage in bovine luteal cells. (7/30793)

To examine hormonal regulation of genes pertinent to luteal steroidogenesis, bovine theca and granulosa cells derived from preovulatory follicles were cultured with various combinations of forskolin and insulin. On Day 8 of culture, progesterone production was measured, and mRNA levels of steroidogenic factor-1 (SF-1), cytochrome P450 side-chain cleavage enzyme (P450scc), and steroidogenic acute regulatory protein (StAR) were determined by means of semiquantitative reverse transcription-polymerase chain reaction. Notably, the combination of forskolin plus insulin stimulated progesterone production in luteinized theca cells. This was probably a result of a synergistic interaction between forskolin and insulin, observed on both StAR and P450scc mRNA levels. However, in luteinized granulosa cells (LGC), forskolin and insulin each independently were able to up-regulate the levels of P450scc and StAR mRNA levels, respectively. Moreover, insulin alone was sufficient to maintain the high steady-state levels of StAR mRNA in LGC. Both insulin and insulin-like growth factor I enhanced StAR gene expression in LGC. SF-1 was constitutively expressed in bovine luteal cells; its amounts did not vary between the two luteal cell types or with hormonal treatments. In summary, this study demonstrates a distinct, cell-type specific regulation of StAR and P450scc mRNA in the two bovine luteal cell types.  (+info)

Plasma total homocysteine and cysteine in relation to glomerular filtration rate in diabetes mellitus. (8/30793)

BACKGROUND: The plasma concentrations of total homocysteine (tHcy) and total cysteine (tCys) are determined by intracellular metabolism and by renal plasma clearance, and we hypothesized that glomerular filtration is a major determinant of plasma tHcy and tCys. We studied the relationships between the glomerular filtration rate (GFR) and plasma tHcy and tCys in populations of diabetic patients with particularly wide ranges of GFR. METHODS: We measured GFR, urine albumin excretion rate (UAER), plasma tHcy, tCys, methionine, vitamin B12, folate, C-peptide, and routine parameters in 50 insulin-dependent diabetes mellitus (IDDM) and 30 non-insulin-dependent diabetes mellitus (NIDDM) patients. All patients underwent intensive insulin treatment and had a serum creatinine concentration below 115 micromol/liter. RESULTS: Mean plasma tHcy in diabetic patients (0.1 micromol/liter) was lower than in normal persons (11.1 micromol/liter, P = 0.0014). Mean plasma tCys in diabetic patients (266.1 micromol/liter) was also lower than in normal persons (281.9 micromol/liter, P = 0.0005). Seventy-three percent of the diabetic patients had relative hyperfiltration. Plasma tHcy and tCys were closely and independently associated with GFR, serum folate, and serum B12. However, plasma tHcy was not independently associated with any of the 22 other variables tested, including age, serum creatinine concentration, UAER, total daily insulin dose, and glycemic control. CONCLUSIONS: Glomerular filtration rate is an independent determinant of plasma tHcy and tCys concentrations, and GFR is rate limiting for renal clearance of both homocysteine and cysteine in diabetic patients without overt nephropathy. Declining GFR explains the age-related increase in plasma tHcy, and hyperfiltration explains the lower than normal mean plasma tHcy and tCys concentrations in populations of diabetic patients.  (+info)

Central Leptin, But Not Central Insulin, Attenuates the Decrease of Adiponectin Concentrations and Increases Insulin...Central Leptin, But Not Central Insulin, Attenuates the Decrease of Adiponectin Concentrations and Increases Insulin...
Central leptin increases peripheral insulin sensitivity through unknown mechanisms. Central insulin signaling may also contribute to peripheral insulin sensitivity. To clarify the relationships among central leptin, central insulin, peripheral insulin sensitivity, and adiponectin, we examined the effects of intracerebroventricular leptin and insulin on peripheral insulin sensitivity and adiponectin concentrations in streptozotocin (STZ)-induced diabetic rats. Rats were cannulated in the lateral ventricle. Intravenous STZ was injected to induce diabetes. After establishment of hyperglycemia in STZ-treated rats, insulin (10 mU/day), leptin (10 µg/day), or vehicle was administered daily for 10 days. After one week of central administration, in vivo insulin sensitivity was measured by injecting IV insulin (0.025 U/kg body weight) and measuring blood glucose concentration 15 minutes after the injection. Rats treated with central leptin had increased peripheral insulin sensitivity. In addition, blood ...
Jikei Optimal Insulin Therapy in Type 2 Diabetes - Full Text View - ClinicalTrials.govJikei Optimal Insulin Therapy in Type 2 Diabetes - Full Text View - ClinicalTrials.gov
The current insulin therapy is divided into the conventional insulin therapy (1~2 injections per day) and the intensive insulin therapy (3~4 injections per day). The kinetics of exogenous insulin in the intensive insulin therapy imitate the kinetics of insulin secretion in a healthy person. A previous large clinical study (e.g. DCCT, Kumamoto study, etc.) suggested that intensive insulin therapy prevented microangiopathy and macroangiopathy, and inhibited progression of them, however many patients chose conventional insulin therapy because many hoped that they injected insulin as few as possible. The patients thought that their life styles were disturbed by many times of insulin injection.. The current dual-acting insulin made from insulin as part modified by protamine is able to suppress postprandial hyperglycemia. The new insulin may possibly have the kinetics of insulin in the patient who uses insulin as the intensive insulin therapy. Moreover, the patients will receive the insulin therapy ...
Effect of insulin therapy on body fat distribution in NIDDM patients with secondary sulfonylurea failure: A preliminary report<...Effect of insulin therapy on body fat distribution in NIDDM patients with secondary sulfonylurea failure: A preliminary report<...
TY - JOUR. T1 - Effect of insulin therapy on body fat distribution in NIDDM patients with secondary sulfonylurea failure. T2 - A preliminary report. AU - Takei, I.. AU - Takayama, S.. AU - Yamauchi, A.. AU - Nakamoto, S.. AU - Kitamura, Y.. AU - Katsukawa, Fuminori. AU - Yamazaki, H.. AU - Saruta, T.. AU - Inoue, S.. PY - 1998/2. Y1 - 1998/2. N2 - Objective: To clarify the influence of insulin therapy on body weight and fat distribution, we compared these parameters in five non-insulin dependent diabetes mellitus (NIDDM) patients, with secondary sulfonylurea failure, before and after insulin therapy. Body weight increased significantly after instituting insulin treatment. However, the visceral to subcutaneous fat (V/S) ratio decreased significantly due to a marked increase in S-fat without a change in V-fat. Insulin therapy necessitated by sulfonylurea failure does not appear to accelerate the atherogenic process in NIDDM patients as there is no increase in visceral fat.. AB - Objective: To ...
Exendin-4 as a stimulator of rat insulin I gene promoter activity via bZIP/CRE interactions sensitive to serine/threonine...Exendin-4 as a stimulator of rat insulin I gene promoter activity via bZIP/CRE interactions sensitive to serine/threonine...
TY - JOUR. T1 - Exendin-4 as a stimulator of rat insulin I gene promoter activity via bZIP/CRE interactions sensitive to serine/threonine protein kinase inhibitor Ro 31-8220. AU - Chepurny, Oleg G.. AU - Hussain, Mehboob. AU - Holz, George G.. PY - 2002. Y1 - 2002. N2 - Signal transduction properties of exendin-4 (Ex-4) underlying its ability to stimulate rat insulin I gene promoter (RIP1) activity were assessed in the pancreatic β-cell line INS-1. Ex-4 acted via glucagon-like peptide-1 receptors to stimulate RIP1 in a glucose-dependent manner, as measured in cells transfected with a -410-bp RIP1-luciferase construct (RIP1-Luc). The action of Ex-4 was independent of cAMP and PKA because it was not blocked by cotransfection with dominant-negative Gαs, was unaffected by pretreatment with the membrane-permeant cAMP antagonist 8-Br-Rp-cAMPS, and remained apparent after treatment with PKA inhibitors H-89 or KT 5720. Similarly, cotransfection with a dominant-negative isoform of the type-2 ...
Glucose-stimulated insulin secretion is coupled to the interaction of actin with the t-SNARE (target membrane soluble N...Glucose-stimulated insulin secretion is coupled to the interaction of actin with the t-SNARE (target membrane soluble N...
TY - JOUR. T1 - Glucose-stimulated insulin secretion is coupled to the interaction of actin with the t-SNARE (target membrane soluble N-ethylmaleimide-sensitive factor attachment protein receptor protein) complex. AU - Thurmond, Debbie C.. AU - Gonelle-Gispert, Carmen. AU - Furukawa, Megumi. AU - Halban, Philippe A.. AU - Pessin, Jeffrey E.. PY - 2003/4/1. Y1 - 2003/4/1. N2 - The actin monomer sequestering agent latrunculin B depolymerized β-cell cortical actin, which resulted in increased glucose-stimulated insulin secretion in both cultured MIN6 β-cells and isolated rat islet cells. In perifused islets, latrunculin B treatment increased both first- and second-phase glucose-stimulated insulin secretion without any significant effect on total insulin content. This increase in secretion was independent of calcium regulation because latrunculin B also potentiated calcium-stimulated insulin secretion in permeabilized MIN6 cells. Confocal immunofluorescent microscopy revealed a redistribution of ...
Insulin index - WikipediaInsulin index - Wikipedia
The Insulin Index of a food represents how much it elevates the concentration of insulin in the blood during the two-hour period after the food is ingested. The index is similar to the Glycemic Index (GI) and Glycemic Load (GL), but rather than relying on blood glucose levels, the Insulin Index is based upon blood insulin levels. The Insulin Index represents a comparison of food portions with equal overall caloric content (250 kcal or 1000 kJ), while GI represents a comparison of portions with equal digestible carbohydrate content (typically 50 g) and the GL represents portions of a typical serving size for various foods. The Insulin Index can be more useful than either the Glycemic Index or the Glycemic Load because certain foods (e.g., lean meats and proteins) cause an insulin response despite there being no carbohydrates present, and some foods cause a disproportionate insulin response relative to their carbohydrate load. Holt et al. have noted that the glucose and insulin scores of most ...
Intensive insulin therapy and mortality among critically ill patients: a meta-analysis including NICE-SUGAR study data | CMAJIntensive insulin therapy and mortality among critically ill patients: a meta-analysis including NICE-SUGAR study data | CMAJ
In our updated meta-analysis of randomized trials of intensive insulin therapy in critically ill patients, we found that such therapy had no effect on the overall risk of death. By including data from the largest trial of intensive insulin therapy, which was recently published,18 we provide the most current and precise estimate of the effect of intensive insulin therapy on mortality and severe hypoglycemia in the ICU setting. We found significant heterogeneity between studies, which was driven primarily by the 2 trials involving surgical patient populations.8,29 In keeping with this observation, our meta-regression analysis suggested that intensive insulin therapy may benefit patients in surgical ICUs. Finally, there was a 6-fold increased risk of severe hypoglycemia among patients given intensive insulin therapy compared with the control treatment. The risk of hypoglycemic events did not differ by type of ICU, or by intensity of insulin therapy.. Our meta-analysis showed a similar overall ...
insulin human insulin human insulin human insulin human insulin - 19395499 - Tenders in Europe | Tendersontimeinsulin human insulin human insulin human insulin human insulin - 19395499 - Tenders in Europe | Tendersontime
Tenders from Ukraine for insulin human insulin human insulin human insulin human insulin human insulin human insulin glulisine insulin glargin insulin glargin insulin human insulin human insulin human insulin human insulin hu.... EuropeThe tender reference number is 19395499 and it is closing on 26th Jan 2019.
Insulin enhances glucose-stimulated insulin secretion in healthy humans<...Insulin enhances glucose-stimulated insulin secretion in healthy humans<...
TY - JOUR. T1 - Insulin enhances glucose-stimulated insulin secretion in healthy humans. AU - Bouche, Clara. AU - Lopez, Ximena. AU - Fleischman, Amy. AU - Cypess, Aaron M.. AU - OShea, Sheila. AU - Stefanovski, Darko. AU - Bergman, Richard N.. AU - Rogatsky, Eduard. AU - Stein, Daniel T.. AU - Kahn, C. Ronald. AU - Kulkarni, Rohit N.. AU - Goldfine, Allison B.. PY - 2010/3/9. Y1 - 2010/3/9. N2 - Islet β-cells express both insulin receptors and insulin-signaling proteins. Recent evidence from rodents in vivo and from islets isolated from rodents or humans suggests that the insulin signaling pathway is physiologically important for glucose sensing. We evaluated whether insulin regulates β-cell function in healthy humans in vivo. Glucose-induced insulin secretion was assessed in healthy humans following 4-h saline (low insulin/sham clamp) or isoglycemic-hyperinsulinemic (high insulin) clamps using B28-Asp insulin that could be immunologically distinguished from endogenous insulin. Insulin and ...
9 Diabetes Statistics and Basal Insulin Facts That May Surprise You9 Diabetes Statistics and Basal Insulin Facts That May Surprise You
Basal insulin therapy is used by people with both type 1 and type 2 diabetes. Glucose is continuously released by the liver throughout the day when there is no food being digested. There are different ways that different types of insulin can mimic the action of this basal insulin in the body.. For people with type 1 and 2 diabetes, long-acting insulin is injected once or twice a day to mimic basal insulin. Those with type 1 would then take insulin to cover mealtimes. Mealtime treatment for type 2 diabetes varies.. For those with type 1 diabetes who are on a pump, quick-acting insulin is delivered at a low rate continuously throughout the day and night, and then a "bolus" amount of insulin is given to cover meals. Using the insulin pump is a good way to adjust the basal insulin levels in a very precise manner. You can program the basal insulin output such that it can match the bodys normal insulin production.. One study looked into the efficacy of basal insulin in being able to improve the A1c ...
A Comparison of the Effects of Selective Increases in Peripheral or Portal insulin on Hepatic Glucose Production in the...A Comparison of the Effects of Selective Increases in Peripheral or Portal insulin on Hepatic Glucose Production in the...
We investigated the mechanisms by which peripheral or portal insulin can independently alter liver glucose production. Isotopic ([3-3H]glucose) and arteriovenous difference methods were used in conscious overnight-fasted dogs. A pancreatic clamp (somatostatin plus basal insulin and basal glucagon infusions) was used to control the endocrine pancreas. After a 40-min basal period, a 180-min experimental period followed in which selective increases in peripheral (PERI group, n = 5) or portal-vein (PORT group, n = 5) insulin were induced. In control dogs (CONT group, n = 10), insulin was not increased. Glucagon levels were fixed in all studies, and basal euglycemia was maintained by peripheral glucose infusion in the two experimental groups. In the PERI group, arterial insulin rose from 36 ± 12 to 120 ± 12 pmol/l, while portal insulin was unaltered. In the PORT group, portal insulin rose from 108 ± 42 to 192 ± 42 pmol/l, while arterial insulin was unaltered. Neither arterial nor portal insulin ...
Patente US7021309 - Method of use of monomeric insulin as a means for improving the ... - Google PatentesPatente US7021309 - Method of use of monomeric insulin as a means for improving the ... - Google Patentes
The need for the delivery of insulin by injection can be reduced or eliminated by delivering an aerosolized monomeric insulin formulation. Repeatability of dosing and more particularly the repeatability of the blood concentration versus time profile is improved relative to regular insulin. The blood concentration versus time profile is substantially unaffected by specific aspects of the patients breathing maneuver at delivery. Further, the rate at which blood glucose is lowered is increased by the use of monomeric insulin. Particles of insulin and in particular monomeric insulin delivered to the surface of lung tissue will be absorbed into the circulatory system. The monomeric insulin may be a dry powder but is preferably in a liquid formulation delivered to the patient from a hand-held, self-contained device which automatically releases an aerosolized burst of formulation. The device includes a sensor which is preferably electronic which measures inspiratory flow and volume which measurement can be
Patent US7021309 - Method of use of monomeric insulin as a means for improving the ... - Google PatentsPatent US7021309 - Method of use of monomeric insulin as a means for improving the ... - Google Patents
The need for the delivery of insulin by injection can be reduced or eliminated by delivering an aerosolized monomeric insulin formulation. Repeatability of dosing and more particularly the repeatability of the blood concentration versus time profile is improved relative to regular insulin. The blood concentration versus time profile is substantially unaffected by specific aspects of the patients breathing maneuver at delivery. Further, the rate at which blood glucose is lowered is increased by the use of monomeric insulin. Particles of insulin and in particular monomeric insulin delivered to the surface of lung tissue will be absorbed into the circulatory system. The monomeric insulin may be a dry powder but is preferably in a liquid formulation delivered to the patient from a hand-held, self-contained device which automatically releases an aerosolized burst of formulation. The device includes a sensor which is preferably electronic which measures inspiratory flow and volume which measurement can be
Insulin Resistance and Insulin Secretory Dysfunction Are Independent Predictors of Worsening of Glucose Tolerance During Each...Insulin Resistance and Insulin Secretory Dysfunction Are Independent Predictors of Worsening of Glucose Tolerance During Each...
Numerous prospective studies in various populations indicate that insulin resistance and insulin secretory dysfunction predict the development of type 2 diabetes (1,2,3,4,5,6). However, the majority of these studies included both individuals with NGT and IGT at baseline and used indirect measures of insulin action and insulin secretion derived from an OGTT. Moreover, to date, only two groups of investigators have examined the metabolic predictors of progression from NGT to IGT (6,8). Thus, although these studies provide evidence for a pathogenic role of insulin resistance and insulin secretory dysfunction in the development of type 2 diabetes, they give only limited information as to the relative importance of these abnormalities during the different stages of the development of the disease.. In the present study, we addressed this question by assessing the predictive effects of insulin resistance and low early-phase insulin secretion separately for the progression from NGT to IGT and also from ...
Effects of type 2 diabetes on the ability of insulin and glucose to regulate splanchnic and muscle glucose metabolism: evidence...Effects of type 2 diabetes on the ability of insulin and glucose to regulate splanchnic and muscle glucose metabolism: evidence...
Insulin-induced stimulation of muscle glucose uptake (MGU) is impaired in people with type 2 diabetes. To determine whether insulin-induced stimulation of splanchnic glucose uptake (SGU) is also impaired, we simultaneously measured leg glucose uptake (LGU) and SGU in 14 nondiabetic subjects and 16 subjects with type 2 diabetes using a combined organ catheterization-tracer infusion technique. Glucose was clamped at approximately 9.3 mmol/l, while insulin concentrations were maintained at approximately 72 pmol/l (low) and approximately 150 pmol/l (high) for 3 h each. Endogenous hormone secretion was inhibited with somatostatin. Total body glucose disappearance was lower (P , 0.01) and glucose production higher (P , 0.01) during both insulin infusions in the diabetic compared with the nondiabetic subjects, indicating insulin resistance. Splanchnic glucose production was higher (P , 0.05) in the diabetic subjects during the low but not the high insulin infusion. SGU was slightly lower in the ...
Autocrine effect of Zn<sup>2+</sup> on the glucose-stimulated insulin...Autocrine effect of Zn<sup>2+</sup> on the glucose-stimulated insulin...
TY - JOUR. T1 - Autocrine effect of Zn2+ on the glucose-stimulated insulin secretion. AU - Slepchenko, Kira G.. AU - Daniels, Nigel A.. AU - Aili, Guo. AU - Li, Yang V.. PY - 2015/9/25. Y1 - 2015/9/25. N2 - It is well known that zinc (Zn2+) is required for the process of insulin biosynthesis and the maturation of insulin secretory granules in pancreatic beta (β)-cells, and that changes in Zn2+ levels in the pancreas have been found to be associated with diabetes. Glucose-stimulation causes a rapid co-secretion of Zn2+ and insulin with similar kinetics. However, we do not know whether Zn2+ regulates insulin availability and secretion. Here we investigated the effect of Zn2+ on glucose-stimulated insulin secretion (GSIS) in isolated mouse pancreatic islets. Whereas Zn2+ alone (control) had no effect on the basal secretion of insulin, it significantly inhibited GSIS. The application of CaEDTA, by removing the secreted Zn2+ from the extracellular milieu of the islets, resulted in significantly ...
A new technique to assess insulin sensitivity in humans: The Rapid Insulin Sensitivity Test (RIST)<...A new technique to assess insulin sensitivity in humans: The Rapid Insulin Sensitivity Test (RIST)<...
TY - JOUR. T1 - A new technique to assess insulin sensitivity in humans. T2 - The Rapid Insulin Sensitivity Test (RIST). AU - Patarrão, Rita S.. AU - Wayne Lautt, W.. AU - Guarino, Maria P.. AU - Afonso, Ricardo A.. AU - Ribeiro, Rogério T.. AU - Fernandes, Ana B.. AU - Boavida, José M.. AU - Macedo, Maria Paula. PY - 2007/12/1. Y1 - 2007/12/1. N2 - The objective of this study was to develop a Rapid Insulin Sensitivity Test (RIST) in humans, a test already used in animal studies. Insulin sensitivity was assessed using a rapid modified euglycemic clamp, the RIST. In this test, glucose disposition was determined after an intravenous (IV) bolus (50mU/kg bw administered over 30 seconds) of insulin, before and after feeding a standardized test meal, in healthy male subjects (aged 27.8±2.4 years, BMI 23.5±1.2 kg/m2). The RIST uses as the index of insulin sensitivity, the total amount of glucose required to be infused to maintain euglycemia during insulin action following an IV bolus of insulin. ...
ERAD-icating mutant insulin promotes functional insulin secretion | Science Translational MedicineERAD-icating mutant insulin promotes functional insulin secretion | Science Translational Medicine
The pancreatic beta cell is an incredible machine producing tens of thousands of insulin molecules every second. When this process works normally, the result is tight regulation of blood glucose and whole body energy stores. However, breakdowns in insulin processing can rapidly overwhelm the beta cell leading to beta cell stress, destruction, and ultimately diabetes. A striking example of this breakdown can be found in the disease MIDY (Mutant INS-gene induced Diabetes of Youth) in which production of a single mutant insulin molecule leads to dominant beta cell failure and diabetes. Now, Cunningham et al. report a potential new pathway that can be exploited to diminish mutant insulin and restore normal insulin secretion.. Misfolded proteins are commonly trapped in the endoplasmic reticulum (ER) where they are triaged by a process known as ER-associated degradation (ERAD) and ultimately destroyed by the cytoplasmic proteasome. Unfortunately, due to insulins capacity to form disulfide bonds, ...
Snails speedy insulin | UNewsSnails' speedy insulin | UNews
Small and speedy. Human insulin is a hormone that is produced in the pancreas and secreted to aid in the bodys uptake of glucose. The insulin molecule consists of an "A" region and a "B" region. Diabetes mellitus disorders arise from impairment of the bodys normal production of insulin. The most effective treatment for diabetes is injection of synthetic insulin.. But a part of the B region causes insulin molecules to stick together and form aggregations of six insulin molecules. Its how insulin is stored in the pancreas. But injected insulin must de-aggregate into individual molecules before doing a person any good - and that process can take up to an hour. The fastest-acting insulin on the market, Humalog, still takes 15-30 minutes to become active. "The ideal scenario would be to take the region off of the B chain" Safavi says. "But then you completely abolish insulin activity.". Chou, Safavi, and colleagues found that insulin produced by the cone snail Conus geographus lacked the segment ...
Insulin Resistance - Why you cant lose weight | DrDekel.comInsulin Resistance - Why you can't lose weight | DrDekel.com
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 ...
Beta-cell-targeted overexpression of phosphodiesterase 3B in mice causes impaired insulin secretion, glucose intolerance and...Beta-cell-targeted overexpression of phosphodiesterase 3B in mice causes impaired insulin secretion, glucose intolerance and...
The second messenger cAMP mediates potentiation of glucose-stimulated insulin release. Use of inhibitors of cAMP-hydrolyzing phosphodiesterase (PDE) 3 and overexpression of PDE3B in vitro have demonstrated a regulatory role for this enzyme in insulin secretion. In this work, the physiological significance of PDE3B-mediated degradation of cAMP for the regulation of insulin secretion in vivo and glucose homeostasis was investigated in transgenic mice overexpressing PDE3B in pancreatic beta-cells. A 2-fold overexpression of PDE3B protein and activity blunted the insulin response to intravenous glucose, resulting in reduced glucose disposal. The effects were "dose"-dependent because mice overexpressing PDE3B 7-fold failed to increase insulin in response to glucose and hence exhibited pronounced glucose intolerance. Also, the insulin secretory response to intravenous glucagon-like peptide 1 was reduced in vivo. Similarly, islets stimulated in vitro exhibited reduced insulin secretory capacity in ...
Patente US20100138453 - System and method for generating a personalized diabetes management tool for ... - Google PatentesPatente US20100138453 - System and method for generating a personalized diabetes management tool for ... - Google Patentes
A system and method for generating a personalized diabetes management tool for diabetes mellitus is provided. An insulin activity curve for a patient population for an insulin preparation for diabetes mellitus treatment is identified. A personal insulin activity model for the patient is generated. An insulin sensitivity is determined by taking a derivative of the rate of change of blood glucose over time for the insulin preparation. An insulin sensitivity coefficient for the insulin preparation for a patient of diabetes mellitus is established. The insulin sensitivity coefficient is applied to the patient population insulin activity curve over a duration of action of the insulin preparation.
Intensive insulin therapy - WikipediaIntensive insulin therapy - Wikipedia
Intensive insulin therapy or flexible insulin therapy is a therapeutic regimen for diabetes mellitus treatment. This newer approach contrasts with conventional insulinotherapy. Rather than minimize the number of insulin injections per day (a technique which demands a rigid schedule for food and activities), the intensive approach favors flexible meal times with variable carbohydrate as well as flexible physical activities. The trade-off is the increase from 2 or 3 injections per day to 4 or more injections per day, which was considered "intensive" relative to the older approach. In North America in 2004, many endocrinologists prefer the term "flexible insulin therapy" (FIT) to "intensive therapy" and use it to refer to any method of replacing insulin that attempts to mimic the pattern of small continuous basal insulin secretion of a working pancreas combined with larger insulin secretions at mealtimes. The semantic distinction reflects changing treatment. Long-term studies like the UK ...
How insulin resistance precedes prediabetes/diabetes and how to detect and manage it | Reverse Diabetes CoachHow insulin resistance precedes prediabetes/diabetes and how to detect and manage it | Reverse Diabetes Coach
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 ...
NEFA elevation during a hyperglycaemic clamp enhances insulin secretion | Garvan Institute of Medical ResearchNEFA elevation during a hyperglycaemic clamp enhances insulin secretion | Garvan Institute of Medical Research
Elevated non-esterified fatty acid (NEFA) levels may influence insulin secretion and contribute to the development of Type 2 DM. We investigated the effects of acute NEFA elevation in controls (n = 6) and subjects predisposed to Type 2 DM (n = 6) on basal insulin levels, and following glucose and arginine stimulation. Each subject had one study with a triglyceride (TG) plus heparin infusion (elevated NEFA levels) and another with normal saline. Twenty minutes after the TG or saline infusion began a glucose bolus was given and 10 min later a 90-min hyperglycaemic clamp (approximately 9 mmol l(-1)) was started. Intravenous arginine was given at 110 min. Elevated NEFA levels (approximately 4000 micromol l(-1)) did not enhance basal or first phase glucose stimulated insulin levels. During hyperglycaemia, NEFA elevation further increased insulin levels in both groups by 20-44% (p | 0.05) and C-peptide levels by 17-25% (p | 0.05). The post-arginine insulin levels during hyperglycaemia were increased by 45% in
Noninsulin-Dependent Diabetes Mellitus Treatment » adminNoninsulin-Dependent Diabetes Mellitus Treatment » admin
589. An individual may get diabetes when the pancreas can no longer secrete the needed hormones that produce insulin. The insulin maintains the glucose in the blood to be normal. Low insulin means that the level of glucose, which is sugar in the blood, may get high and may lead to diabetes.. The autoimmune reaction is a type 1 diabetes where the cells in the pancreas organ that produces the needed insulin are destroyed. This results to the total loss of insulin in the hormones. …. diabetes. An individual may get diabetes when the pancreas can no longer secrete the needed hormones that produce insulin. The insulin maintains the glucose in the blood to be normal. Low insulin means that the level of glucose, which is sugar in the blood, may get high and may lead to diabetes.. The autoimmune reaction is a type 1 diabetes where the cells in the pancreas organ that produces the needed insulin are destroyed. This results to the total loss of insulin in the hormones. This happens because the body has ...
Changes in fetal mannose and other carbohydrates induced by a maternal insulin infusion in pregnant sheep | Journal of Animal...Changes in fetal mannose and other carbohydrates induced by a maternal insulin infusion in pregnant sheep | Journal of Animal...
The importance of non-glucose carbohydrates, especially mannose and inositol, for normal development is increasingly recognized. Whether pregnancies complicated by abnormal glucose transfer to the fetus also affect the regulation of non-glucose carbohydrates is unknown. In pregnant sheep, maternal insulin infusions were used to reduce glucose supply to the fetus for both short (2-wk) and long (8-wk) durations to test the hypothesis that a maternal insulin infusion would suppress fetal mannose and inositol concentrations. We also used direct fetal insulin infusions (1-wk hyperinsulinemic-isoglycemic clamp) to determine the relative importance of fetal glucose and insulin for regulating non-glucose carbohydrates. A maternal insulin infusion resulted in lower maternal (50%, P | 0.01) and fetal (35-45%, P | 0.01) mannose concentrations, which were highly correlated (r2 = 0.69, P | 0.01). A fetal insulin infusion resulted in a 50% reduction of fetal mannose (P | 0.05). Neither maternal nor fetal plasma
Chronic insulin treatment of diabetes does not fully normalize alterations in the retinal transcriptome | BMC Medical Genomics ...Chronic insulin treatment of diabetes does not fully normalize alterations in the retinal transcriptome | BMC Medical Genomics ...
Diabetic retinopathy (DR) is a leading cause of blindness in working age adults. Approximately 95% of patients with Type 1 diabetes develop some degree of retinopathy within 25 years of diagnosis despite normalization of blood glucose by insulin therapy. The goal of this study was to identify molecular changes in the rodent retina induced by diabetes that are not normalized by insulin replacement and restoration of euglycemia. The retina transcriptome (22,523 genes and transcript variants) was examined after three months of streptozotocin-induced diabetes in male Sprague Dawley rats with and without insulin replacement for the later one and a half months of diabetes. Selected gene expression changes were confirmed by qPCR, and also examined in independent control and diabetic rats at a one month time-point. Transcriptomic alterations in response to diabetes (1376 probes) were clustered according to insulin responsiveness. More than half (57%) of diabetes-induced mRNA changes (789 probes) observed at
Ultra-Rapid Acting Insulin - ArecorUltra-Rapid Acting Insulin - Arecor
There is a recognised need to develop insulin products with faster onset of action compared with the current state-of-the-art prandial insulin products. Prandial insulin is used by diabetics to control the blood glucose rise after meals. To ensure effective blood glucose management it is essential that, once injected, insulin begins to act as rapidly as possible. Whilst there has been good progress in developing rapid acting insulins in the last two decades, there is a strong need to develop products that are even more rapid-acting to ensure lower variability of post-meal blood glucose elevations and lower rates of hypoglycaemia. Ultra-rapid acting insulin is also a key component required for the development of efficient closed-loop pump systems that would enable automatic glucose control based on a combination of continuous glucose measurement, smart algorithms to decide how much insulin ultra-rapid acting insulin to deliver via an insulin pump. The rapidity of response is critical in such ...
Plasma (or Serum) Insulin Assay - Articles on Medical Diseases and ConditionsPlasma (or Serum) Insulin Assay - Articles on Medical Diseases and Conditions
Insulin was the first hormone measured successfully by radioisotope immunoassay, and insulin assay is now available in most sizable reference laboratories. Insulin is excreted primarily through the kidneys. In general, juvenile diabetics have low fasting insulin levels, and an OGTT using insulin determinations usually produces a flat curve. Mild diabetics have normal fasting insulin levels and display an insulin GTT curve that has a delayed rise, either to normal height or to a point moderately above normal; in either case the curve thereafter falls in a normal fashion. Decreased tolerance due to many other causes produces similar curves; an insulin OGTT has not been more efficient in uncovering subclinical diabetes than blood glucose OGTT. Some maintain that the ratio of insulin values to glucose values obtained on the same specimen during the OGTT is more reliable than insulin values alone. At any rate, most investigators believe that, at present, plasma insulin levels should not be used for ...
Inhibition of cyclooxygenases attenuates diet-induced obesity and compensatory increased glucose-stimulated insulin secretion...Inhibition of cyclooxygenases attenuates diet-induced obesity and compensatory increased glucose-stimulated insulin secretion...
Obesity is considered a state of low-grade inflammation, and this inflammation is strongly related to development of systematic insulin resistance. Hyperglycemia develops during insulin resistance as insulin-stimulated glucose uptake in peripheral insulin sensitive tissues is reduced. Hepatic insulin resistance is often accompanied with increased gluconeogenesis and increased hepatic glucose output, which further increase blood glucose. To cope with the hyperglycemia, the pancreatic -cells compensate by increasing insulin secretion. However, after a certain amount of time, the -cells are no longer able to compensate, and insulin production stops. This may be accompanied with apoptosis in the -cells. Indomethacin is an NSAID and a non-selective inhibitor of cyclooxygenase 1 (COX-1) and 2 (COX-2). In this study we have demonstrated that COX-inhibition using indomethacin, attenuated high fat/high sucrose-induced obesity in C57BL/6J mice. Obesity and glucose intolerance ...
Long-term preoperative glycemic control restored the perioperative neutrophilic phagocytosis activity in diabetic mice | BMC...Long-term preoperative glycemic control restored the perioperative neutrophilic phagocytosis activity in diabetic mice | BMC...
The risk of surgical site infection has been reported to be higher in patients with poorly controlled diabetes. Since chronic hyperglycemia impairs neutrophil functions, preoperative glycemic control may restore neutrophil function. However, long-term insulin therapy may lead to a delay in surgery, which may be a problem, especially in cancer surgery. It is therefore unfortunate that there have been few studies in which the optimal duration of perioperative glycemic control for diabetes with chronic hyperglycemia was investigated. Therefore, we investigated the effects of preoperative long-term insulin therapy and short-term insulin therapy on perioperative neutrophil functions in diabetic mice with chronic hyperglycemia. Five-week-old male C57BL/6 J mice were divided into four groups (No insulin (Diabetes Mellitus: DM), Short-term insulin (DM), Long-term insulin (DM), and Non-diabetic groups). Diabetes was established by administrating repeated low-dose streptozotocin. The Short-term insulin (DM) group
Zn2+ chelation by serum albumin improves hexameric Zn2+-insulin dissociation into monomers after exocytosis. | Physicians...Zn2+ chelation by serum albumin improves hexameric Zn2+-insulin dissociation into monomers after exocytosis. | Physician's...
β-cells release hexameric Zn2+-insulin into the extracellular space, but monomeric Zn2+-free insulin appears to be the only biologically active form. The mechanisms implicated in dissociation of the hexamer remain unclear, but they seem to be Zn2+ concentration-dependent. In this study, we investigate the influence of albumin binding to Zn2+ on Zn2+-insulin dissociation into Zn2+-free insulin and its physiological, methodological and therapeutic relevance. Glucose and K+-induced insulin release were analyzed in isolated mouse islets by static incubation and perifusion experiments in the presence and absence of albumin and Zn2+ chelators. Insulin tolerance tests were performed in rats using different insulin solutions with and without Zn2+ and/or albumin. Albumin-free buffer does not alter quantification by RIA of Zn2+-free insulin but strongly affects RIA measurements of Zn2+-insulin. In contrast, accurate determination of Zn2+-insulin was obtained only when bovine serum albumin or Zn2+ ...
Effects of duration of type 2 diabetes mellitus on insulin secretion<...Effects of duration of type 2 diabetes mellitus on insulin secretion<...
TY - JOUR. T1 - Effects of duration of type 2 diabetes mellitus on insulin secretion. AU - Zangeneh, Farhad. AU - Arora, Puneet S.. AU - Dyck, Peter J.. AU - Bekris, Lynn. AU - Lernmark, Ake. AU - Achenbach, Sara J.. AU - Oberg, Ann L.. AU - Rizza, Robert A.. PY - 2006. Y1 - 2006. N2 - Objective: To gain insight into the effects of duration of type 2 diabetes on insulin secretion in patients with type 2 diabetes mellitus. Methods: C-peptide concentrations were measured every 2 years before and after intravenous injection of 1 mg of glucagon in 89 patients with type 2 diabetes (51 men and 38 women) as part of the Rochester Diabetic Neuropathy Study in those subjects who participated in follow-up (median, 12 years; range, 6 to 14). Results: Although insulin secretion decreased over time (P,0.001) in the group as a whole, both the pattern and the rate of decline in C-peptide concentration differed considerably among the study subjects. Insulin secretion, whether measured as fasting C-peptide, ...
InsulinInsulin
Different people need different types of insulin, so your treatment needs to be tailored to suit you. Your GP-or an endocrinologist-will prescribe the insulin that best suits your lifestyle and blood glucose level targets and advise you on how to use this insulin properly.. The different types of insulin are grouped together based on how long the insulin works in the body. There are five types of insulin (see table below). Insulin can be given as a basal or bolus dose. Basal insulin is a background insulin (intermediate or long acting). Bolus insulin is an ultra-short or short-acting insulin that is usually given with meals.. You may be prescribed more than one type of insulin depending on the type of diabetes you have and your individual management plan. Your insulin needs can also change over time, so its important to have regular reviews of your diabetes management with your GP or CDE. ...
Insulin Strategies for Primary Care Providers | Clinical DiabetesInsulin Strategies for Primary Care Providers | Clinical Diabetes
The same flexible insulin regimens used in patients with type 1 diabetes are also used in patients with type 2 diabetes. Intermediate-acting (basal) insulin may be administered at bedtime, although it is usually used twice daily. Some use it more frequently. Prandial insulin is provided by rapid- or short-acting insulin administered with each meal. In type 1 diabetes, patients weight is used to determine the total amount of insulin needed as 0.4-0.8 units/kg/day, although some women may require less than this amount. Patients with type 2 diabetes frequently require ,1.0 unit/kg/day. As a rule of thumb, approximately half of the total daily insulin dose is basal insulin.. With NPH-based regimens, it becomes difficult to separate the basal from the prandial insulin because NPH may act as both. For example, if NPH is administered in the morning, it would serve as basal insulin in the late morning after breakfast is absorbed, as prandial insulin partly if not totally responsible for the lunch meal, ...
Challenging the dogma: Tissue specific regulation of insulin actionChallenging the dogma: Tissue specific regulation of insulin action
A role for glucocorticoids (GCs) in the regulation of carbohydrate metabolism and the development of diabetes was first described over 70 years ago. Whilst there is little doubt that systemic GC excess leads to insulin resistance the tissue specific mechanisms underpinning their effect on insulin sensitivity remain to be understood. We have defined tissue specific effects of GCs on insulin sensitivity and lipid metabolism in vitro and in vivo. In skeletal myotubes GCs, in the absence of insulin, decreased glucose uptake and de novo lipogenesis and increased β-oxidation. GC treatment caused insulin resistance, demonstrated by inhibition of insulin signalling and impaired glucose uptake. In human adipocytes, the direct effects of GCs were similar to those in myotubes, with decreased basal glucose uptake and de novo lipogenesis. However, GCs enhanced insulin signalling, insulin-stimulated glucose uptake and de novo lipogenesis. This represents the first description of GC induced insulin ...
Insulin is a carcinogen | Dr. William DavisInsulin is a carcinogen | Dr. William Davis
The science is clear: Insulin is carcinogenic.. People with insulin resistance, metabolic syndrome/pre-diabetes, and type 2 diabetes have high levels of blood insulin, typically many times higher than normal. People with these conditions are at increased risk for various cancers such as breast, colon, prostate, and pancreas (Gallagher 2015). Type 2 diabetics are also more likely to die of their cancer than non-diabetics. While the cause-effect connection is due to a number of factors (high blood sugar, inflammation, high circulating estrogen levels, increased insulin-like growth factors, etc.), much of the increased cancer risk is due to increased levels of insulin.. So what drug is commonly prescribed to people with type 2 diabetes who already have high insulin levels? More insulin. Injected insulin further raises blood insulin levels in people who start with high insulin levels. What would you predict would be the result? You got it: lots more cancer (Hemkens 2009; Suissa 2011). Risk appears ...
Pathophysiology of Insulin Secretion in Non-insulin-dependent Diabetes Mellitus | Diabetes CarePathophysiology of Insulin Secretion in Non-insulin-dependent Diabetes Mellitus | Diabetes Care
The pathogenesis of the abnormal metabolic state in patients with non-insulin-dependent diabetes (NIDDM) is controversial. Even the term NIDDM stirs controversy because of the easily drawn inference that individuals with this form of diabetes do not need insulin treatment. Yet many patients with NIDDM are treated with insulin; some even develop hyperosmolar coma if not given insulin. Ketoacidosis, however, is very infrequent in this syndrome, implying that these patients are not dependent on insulin treatment to prevent mass mobilization of fatty acids and ketone bodies. The phrase noninsulin-dependent is therefore appropriate when used in this restricted fashion but inappropriate when used to imply adequacy of insulin secretion. The evaluation of the adequacy of islet function in this syndrome has been complex, since there is no standard of insulin output that can be defined for normal islets without specifying the physiologic setting under which the assessment has been made. For example, ...
Insulin Basics | ADAInsulin Basics | ADA
Inside the pancreas, the hormone insulin is made in the beta cells, which are part of the Islets of Langerhans. These islets also have alpha cells, which make glucagon, as well as delta cells. With each meal, beta cells release insulin to help the body use or store the blood sugar it gets from food.. In the beta cells, insulin is created first as a big molecule called "proinsulin." Proinsulin is broken into two pieces: insulin and C-peptide. C-peptide is important especially when determining treatment because it can be used to measure how much insulin a person is making. The more C-peptide a person has, the more insulin they are making. This can help a provider determine how much insulin to prescribe. In people with type 1 diabetes, the pancreas no longer makes insulin. The beta cells have been destroyed and they need insulin shots to use glucose from meals.. People with type 2 diabetes make insulin, but their bodies dont respond well to it. Some people with type 2 diabetes need diabetes pills ...
Insulin receptor phosphorylation may not be a prerequisite for acute insulin action<...Insulin receptor phosphorylation may not be a prerequisite for acute insulin action<...
TY - JOUR. T1 - Insulin receptor phosphorylation may not be a prerequisite for acute insulin action. AU - Simpson, Ian A.. AU - Hedo, José A.. PY - 1984/1/1. Y1 - 1984/1/1. N2 - An antiserum to the insulin receptor mimicked insulins acute actions on glucose transport, phosphorylation of integral membrane proteins, and internalization of the insulin receptor in isolated rat adipose cells. These insulinomimetic actions of the antiserum occurred without the equivalent increase in phosphorylation of the β subunit of the insulin receptor observed with insulin. Thus, a role of receptor phosphorylation in acute insulin action is now questioned.. AB - An antiserum to the insulin receptor mimicked insulins acute actions on glucose transport, phosphorylation of integral membrane proteins, and internalization of the insulin receptor in isolated rat adipose cells. These insulinomimetic actions of the antiserum occurred without the equivalent increase in phosphorylation of the β subunit of the insulin ...
Serval - A radioimmunoassay for human insulin receptor correlation between insulin binding and receptor massServal - A radioimmunoassay for human insulin receptor correlation between insulin binding and receptor mass
We have developed a radioimmunoassay for human insulin receptor. Serum from a patient with Type B severe insulin resistance was used as anti-insulin receptor antiserum. Pure human placental insulin receptor was used as reference preparation and 125I labeled pure insulin receptor as trace. The radioimmunoassay was sensitive (limit of detection less than 17 fmol), reproducible (inter and intra-assay coefficients of variation 12.5% and 1.6% respectively) and specific (no crossreactivity with pure placental IGF-1 receptor, insulin and glucagon). The anti-insulin receptor antibody was, however, able to differentiate between insulin receptor from human placenta and from rat liver. To determine the number of insulin binding sites per receptor, we measured insulin binding (by insulin binding assay) and insulin receptor mass (by radioimmunoassay) in solubilized aliquots from 5 human placentas. The molar ratio of insulin binding to receptor mass was 0.86 +/- 0.12 when binding was determined with
Determinants of intensive insulin therapeutic regimens in patients with type 1 diabetes : data from a nationwide multicenter...Determinants of intensive insulin therapeutic regimens in patients with type 1 diabetes : data from a nationwide multicenter...
Background: To evaluate the determinants of intensive insulin regimens (ITs) in patients with type 1 diabetes (T1D). Methods: This multicenter study was conducted between December 2008 and December 2010 in 28 public clinics in 20 Brazilian cities. Data were obtained from 3,591 patients (56.0% female, 57.1% Caucasian). Insulin regimens were classified as follows: group 1, conventional therapy (CT) (intermediate human insulin, one to two injections daily); group 2 (three or more insulin injections of intermediate plus regular human insulin); group 3 (three or more insulin injections of intermediate human insulin plus short-acting insulin analogues); group 4, basal-bolus (one or two insulin injections of long-acting plus short-acting insulin analogues or regular insulin); and group 5, basal-bolus with continuous subcutaneous insulin infusion (CSII). Groups 2 to 5 were considered IT groups. Results: We obtained complete data from 2,961 patients. Combined intermediate plus regular human insulin was ...
Serum insulin concentrations, insulin sensitivity, and endothelial function in essential hypertension and non-insulin-dependent...Serum insulin concentrations, insulin sensitivity, and endothelial function in essential hypertension and non-insulin-dependent...
A series of studies is described in which specific and conventional insulin immunoassays, the hyperinsulinaemic clamp technique and forearm venous occlusion plethysmography with local intra-arterial infusions have been used to investigate: the effect of insulin assay specificity on the relationships among serum insulin concentrations, insulin sensitivity, and blood pressure in diabetic and non-diabetic subjects with and without essential hypertension (Chapter 5) the effect of sustained physiological activation of the renin-angiotensin system induced by moderate dietary sodium restriction on insulin sensitivity in patients with non-insulin-dependent diabetes mellitus (Chapter 6) the relationship between endothelial function and insulin sensitivity in healthy subjects (Chapter 7) Prior to these investigations, preliminary studies (Chapters 3 and 4) were performed in order to validate aspects of the clinical physiological techniques required for the measurement of blood flow and insulin ...
Free fatty acid-induced peripheral insulin resistance augments splanchnic glucose uptake in healthy humans<...Free fatty acid-induced peripheral insulin resistance augments splanchnic glucose uptake in healthy humans<...
TY - JOUR. T1 - Free fatty acid-induced peripheral insulin resistance augments splanchnic glucose uptake in healthy humans. AU - Bajaj, Mandeep. AU - Berria, Rachele. AU - Pratipanawatr, Thongchai. AU - Kashyap, Sangeeta. AU - Pratipanawatr, Wilailak. AU - Belfort, Renata. AU - Cusi, Kenneth. AU - Mandarino, Lawrence. AU - Defronzo, Ralph A.. PY - 2002. Y1 - 2002. N2 - To investigate the effect of elevated plasma free fatty acid (FFA) concentrations on splanchnic glucose uptake (SGU), we measured SGU in nine healthy subjects (age, 44 ± 4 yr; body mass index, 27.4 ± 1.2 kg/m2; fasting plasma glucose, 5.2 ± 0.1 mmol/l) during an Intralipid-heparin (LIP) infusion and during a saline (Sal) infusion. SGU was estimated by the oral glucose load (OGL)insulin clamp method: subjects received a 7-h euglycemic insulin (100 mU·m-2·min-1) clamp, and a 75-g OGL was ingested 3 h after the insulin clamp was started. After glucose ingestion, the steady-state glucose infusion rate (GIR) during the insulin ...
Difference between revisions of Palmeira 2019 MiP2019 - BioblastDifference between revisions of "Palmeira 2019 MiP2019" - Bioblast
Chronic insulin treatment in both cell lines (C2C12 and Huh7) causes a decrease in phosphorylation of Akt, which is a hallmark of insulin resistance at the cellular level. The same effect was observed in both cell lines after chronic palmitate treatment. Chronic insulin treatment does not affect viability of (C2C12 and Huh7), while palmitate treatment decreases cell viability in both cell types. Chronic insulin treatment does not affect mitochondrial respiration, at variance with chronic palmitate treatment, which decreases respiration in C2C12 and Huh7 cells. However, chronic insulin treatment causes a decrease in respiratory acceptor control ratio (RCR) in C2C12, as observed with palmitate treatment. This is not the case for Huh7 cells, where RCR is unchanged after insulin treatment, while lowered only after palmitate treatment. Total ROS production does not change significantly in either cell line. Both C2C12 and Huh7 cells showed preserved mitochondrial morphology after chronic insulin ...
Dose-response characteristics for effects of insulin on production and utilization of glucose in man.<...Dose-response characteristics for effects of insulin on production and utilization of glucose in man.<...
TY - JOUR. T1 - Dose-response characteristics for effects of insulin on production and utilization of glucose in man.. AU - Rizza, R. A.. AU - Mandarino, L. J.. AU - Gerich, J. E.. PY - 1981/6/1. Y1 - 1981/6/1. N2 - To determine the dose-response characteristics for the effects of insulin on glucose production, glucose utilization, and overall glucose metabolism in normal man, 15 healthy subjects were infused with insulin for 8 h at sequential rates ranging from 0.2 to 5.0 mU.kg-1.min-1; each rate was used for 2 h. Glucose production and utilization were measured isotopically ([3-3H]glucose). Tissue insulin receptor occupancy was estimated from erythrocyte insulin binding. Glucose production was completely suppressed at plasma insulin concentrations of approximately 60 microunits/ml. Maximal glucose utilization (10-11 mg.kg-1.min-1) occurred at insulin concentrations of 200-700 microunits/ml. The concentration of insulin causing half-maximal glucose utilization (55 + 7 microunits/ml) was ...
Membrane-targeted phosphatidylinositol 3-kinase mimics insulin actions and induces a state of cellular insulin resistance<...Membrane-targeted phosphatidylinositol 3-kinase mimics insulin actions and induces a state of cellular insulin resistance<...
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) ...
ACCU CHEK FlexLink Plus Insulin System Injury Lawyer | ACCU CHEK FlexLink Plus Insulin System Attorney | ACCU CHEK FlexLink...ACCU CHEK FlexLink Plus Insulin System Injury Lawyer | ACCU CHEK FlexLink Plus Insulin System Attorney | ACCU CHEK FlexLink...
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Microtubules act as cellular rheostat to control insulin secretion | Vanderbilt News | Vanderbilt UniversityMicrotubules act as cellular 'rheostat' to control insulin secretion | Vanderbilt News | Vanderbilt University
Microtubules - cellular "highways" that deliver cargo to the cell membrane for secretion - have a surprising role in pancreatic beta cells. Instead of facilitating glucose-stimulated insulin secretion, they limit it, a team of Vanderbilt investigators reported recently in Developmental Cell.. The findings reveal that microtubules act as a cellular "rheostat" to precisely control insulin secretion and suggest that disturbance of this control may contribute to beta cell dysfunction and type 2 diabetes. Targeting the microtubule regulation of insulin secretion may offer new ways to treat diabetes.. Irina Kaverina, Ph.D., Xiadong Zhu, Ph.D., and colleagues began using pancreatic beta cells as a model to study microtubule function - to explore how microtubules "traffic" cargo such as insulin granules from the cell interior to the periphery.. In their initial studies, the researchers used compounds to destroy the microtubules, then stimulated the pancreatic islets with glucose and measured how much ...
The in vivo interaction between gliclazide and glibenclamide and insulin on glucose disposal in the rat<...The in vivo interaction between gliclazide and glibenclamide and insulin on glucose disposal in the rat<...
TY - JOUR. T1 - The in vivo interaction between gliclazide and glibenclamide and insulin on glucose disposal in the rat. AU - Tanira, Musbah O M. AU - Furman, Brian L.. PY - 1999/5. Y1 - 1999/5. N2 - Many reports suggest that extrapancreatic actions contribute to the antidiabetic effect of sulphonylurea drugs (SUs). In this work, the ability of two SUs, namely, gliclazide and glibenclamide, to augment insulin action was studied in vivo. Both drugs elevated the plasma concentration of immunoreactive insulin (IRI) and lowered the plasma concentrations of glucose and non-esterified fatty acids (NEFA) in normal intact rats. These changes were not reproduced in alloxan-diabetic or eviscerated rats. The actions of insulin on plasma glucose and NEFA were not augmented by gliclazide in alloxan-diabetic rats. Neither gliclazide nor glibenclamide (given acutely and for 30 days) augmented the actions of exogenously administered insulin in reducing plasma glucose or NEFA concentrations in intact or ...
A comparative study of amino acid consumption by rat islet cells and the clonal beta-cell line BRIN-BD11 - the functional...A comparative study of amino acid consumption by rat islet cells and the clonal beta-cell line BRIN-BD11 - the functional...
TY - JOUR. T1 - A comparative study of amino acid consumption by rat islet cells and the clonal beta-cell line BRIN-BD11 - the functional significance of L-alanine. AU - Dixon, G. AU - Nolan, J. AU - McClenaghan, Neville. AU - Flatt, Peter. AU - Newsholme, P. PY - 2003/12. Y1 - 2003/12. N2 - Evidence has been published that L-alanine may, under appropriate conditions, promote insulin secretion in normal rodent islets and various beta cell lines. Previous results utilising the clonal beta-cell line BRIN-BD11, demonstrated that alanine dramatically elevated insulin release by a mechanism requiring oxidative metabolism. We demonstrate in this paper that addition Of L-alanine had an insulinotropic effect in dispersed primary islet cells. Addition Of D-glucose increased L-alanine consumption in both BRIN-BD11 cells and primary islet cells. L-glutamine consumption in the BRIN-BD11 cell line and primary rat islets was also determined. The consumption rate was in line with that previously reported for ...
Pathophysiology of hyperinsulinemia following pancreas transplantation: Altered pulsatile versus basal insulin secretion and...Pathophysiology of hyperinsulinemia following pancreas transplantation: Altered pulsatile versus basal insulin secretion and...
TY - JOUR. T1 - Pathophysiology of hyperinsulinemia following pancreas transplantation. T2 - Altered pulsatile versus basal insulin secretion and the role of specific transplant anatomy in dogs. AU - Earnhardt, Richard C.. AU - Veldhuis, Johannes D. AU - Cornett, Greg. AU - Hanks, John B.. AU - Andersen, Dana K.. AU - Brunicardi, F. Charles. AU - Thomas, Francis T.. AU - Najarian, John S.. PY - 2002/10. Y1 - 2002/10. N2 - Objective: To evaluate the effect of the anatomical alterations of the pancreas required for transplantation on pulsatile insulin secretion. Summary Background Data: Pancreas transplantation involves anatomical changes that have unknown consequences on glucose homeostasis. Pancreas transplant patients are free of exogenous insulin requirements, yet appear to have endogenous hyperinsulinemia. The effect of surgical alterations on posttransplant insulin release is not completely known, specifically with regards to possible alterations in patterns of pulsatile release. Methods: ...
SAD-A Potentiates Glucose-Stimulated Insulin Secretion as a Mediator of Glucagon-Like Peptide 1 Response in Pancreatic β Cells<...SAD-A Potentiates Glucose-Stimulated Insulin Secretion as a Mediator of Glucagon-Like Peptide 1 Response in Pancreatic β Cells<...
TY - JOUR. T1 - SAD-A Potentiates Glucose-Stimulated Insulin Secretion as a Mediator of Glucagon-Like Peptide 1 Response in Pancreatic β Cells. AU - Nie, Jia. AU - Lilley, Brendan N.. AU - Pan, Y. Albert. AU - Faruque, Omar. AU - Liu, Xiaolei. AU - Zhang, Weiping. AU - Sanes, Joshua R.. AU - Han, Xiao. PY - 2013/7/1. Y1 - 2013/7/1. N2 - Type 2 diabetes is characterized by defective glucose-stimulated insulin secretion (GSIS) from pancreatic cells, which can be restored by glucagon-like peptide 1 (GLP-1), an incretin hormone commonly used for the treatment of type 2 diabetes. However, molecular mechanisms by which GLP-1 affects glucose responsiveness in islet β cells remain poorly understood. Here we investigated a role of SAD-A, an AMP-activated protein kinase (AMPK)-related kinase, in regulating GSIS in mice with conditional SAD-A deletion. We show that selective deletion of SAD-A in pancreas impaired incretins effect on GSIS, leading to glucose intolerance. Conversely, overexpression of ...
Different Insulin Therapies - Igabbiani Diabetes Hba1cDifferent Insulin Therapies - Igabbiani Diabetes Hba1c
Joslin_Medalist_Application_2013.doc. Different Insulin Therapies juvenile diabetes research foundation new jersey Divulge does lack of vitamin d cause diabetes. Detectable Pancreatic Lesions Common in People at High Risk for Unlike screening for colon cancer pancreatic cancer screening is not recommended for the Urine test parameters. Insulin NPH INSULIN IS NOT Insulin type: Insulin Brand: Starts in (onset) Peaks in Australia and The Cat Clinic Mt Gravatt Brisbane Australia. the fact that its winter you nose at night = dry mouth Learn more about our Neuropathy Treatment Center. diabetes cause gum disease diabetic fruit list Read More; diabetes education programs diabetes education programs Read More; risk factors for diabetes mellitus Shop online or at three Winnipeg locations: RX Shoe Finder; Size Guide; Diabetic fried rice with pork fillet Socks; Orthopedic goods; Handbags; Treatment For Type 2 Herpes :: Diabetes Drug Urine - The 3 Step Trick that Reverses Diabetes Permanently in As Little ...
Continuous Perioperative Insulin Infusion Decreases Major Cardiovascular Events in Patients Undergoing Vascular Surgery:A...Continuous Perioperative Insulin Infusion Decreases Major Cardiovascular Events in Patients Undergoing Vascular Surgery:A...
Patients were randomly assigned, using a 1:1 block randomization scheme, to either the experimental protocol using a continuous insulin infusion (CII) protocol (1) or to the control group using a standard intermittent sliding-scale insulin bolus (IIB) protocol (2). In the CII regimen, the target blood glucose concentration was 100-150 mg/dl. If blood glucose levels exceeded 150 mg/dl, a continuous insulin infusion was initiated. Adjustments to the insulin infusion were determined by both the current blood glucose concentrations and insulin infusion rates and as specified in 1. Changes in the insulin infusion rate were made by the anesthesiologist in the operating room and by the patients nurse in the postanesthetic care unit and vascular intensive care unit. This protocol had previously been evaluated and shown to achieve blood glucose concentrations within the target range in more than 70% of patients.9 Blood glucose levels were measured in the CII group every hour until stable. Blood glucose ...
Appearance of glucose-induced insulin release in fetal rat β-cellsAppearance of glucose-induced insulin release in fetal rat β-cells
Fetal rat pancreatic cells were isolated from pancreatic primordia on days 12-14 of pregnancy and cultured for 48 h in the presence of 5 mmol/l glucose. Insulin accumulation in the medium over the next 24 h was measured. Cultured cells from day 12 fetuses secreted about 1 fmol insulin per pancreas in response to 5 or 15 mmol/l glucose irrespective of whether 1 mmol/l tolbutamide, 400 mumol/l diazoxide, 5 mmol/l theophylline or 10 mmol/l mannoheptulose was present. In contrast, insulin released from day 13 cultured cells increased significantly from 3.0 +/- 0.6 to 6.2 +/- 2.2 fmol per pancreas, when the glucose concentration was raised. Tolbutamide increased, diazoxide and mannoheptulose decreased and theophylline had no effect on insulin release. Even more pronounced effects were found on insulin release from day 14 cultured cells, in which theophylline also increased the release. In addition, insulin release from cells from pregnancy day 14 was 75 +/- 16 amol/min per pancreas when the cells ...
The effect of xylazine and xylazine followed by insulin on blood glucose and insulin in the dairy cow | Veterinary RecordThe effect of xylazine and xylazine followed by insulin on blood glucose and insulin in the dairy cow | Veterinary Record
The effect of xylazine and xylazine followed 20 minutes later by insulin upon glucose metabolism and plasma insulin concentrations was examined in three cows. After doses of 0.18 mg per kg xylazine given intramuscularly (IM) or 0.15 mg per kg given intravenously (IV) hepatic glucose production increased, plasma insulin concentrations decreased to 25 to 33 per cent of control values, and there was a prolonged hyperglycaemia. When 200 units of soluble insulin were given 20 minutes after similar doses of xylazine there was a rapid fall in blood glucose and a reduction in the rate of glucose production by the liver. Xylazine-induced hyperglycaemia arose from a combination of increased hepatic glucose production and reduced plasma insulin concentrations. Peripheral tissues were still responsive to insulin and when adequate insulin was available blood glucose concentrations rapidly decreased.. ...
IP] NEW ANALOG INSULIN....GLARGINEIP] NEW ANALOG INSULIN....GLARGINE
New Insulin Analog The first of possibly 2 new insulin analogs to be introduced this year was approved by the FDA in late April. Insulin glargine is an insulin analog produced by recombinant DNA technology. A glycine substitution on the A-chain and the extension on the B-chain of 2 arginine residues creates a shift in the isoeletric point, reducing the aqueous solubility of this insulin at physiologic pH. Furthermore, the hexomeric structure of this molecule is stabilized which causes a delay in the dissociation into monomers. Consequently, insulin glargine has a delayed and prolonged absorption.The absorption of insulin glargine is flat and lasts 24 hours. Perhaps even more importantly, the absorption is more consistent, compared with the other commonly used basal insulins, NPH and Ultralente. The need to separate basal from prandial insulins will continue to become more important as insulin therapies for type 1 diabetes continues to evolve.Studies for insulin glargine show 1 common theme -- a ...
Defects in insulin receptor signaling in vivo in the polycystic ovary syndrome (PCOS)<...Defects in insulin receptor signaling in vivo in the polycystic ovary syndrome (PCOS)<...
TY - JOUR. T1 - Defects in insulin receptor signaling in vivo in the polycystic ovary syndrome (PCOS). AU - Dunaif, Andrea. AU - Wu, Xinqi. AU - Lee, Anna. AU - Diamanti-Kandarakis, Evanthia. PY - 2001/8/27. Y1 - 2001/8/27. N2 - Women with polycystic ovary syndrome (PCOS) are insulin resistant secondary to a postbinding defect in insulin signaling. Sequential euglycemic glucose clamp studies at 40 and 400 mU·m-2·min-1 insulin doses with serial skeletal muscle biopsies were performed in PCOS and age-, weight-, and ethnicity-matched control women. Steady-state insulin levels did not differ, but insulin-mediated glucose disposal was significantly decreased in PCOS women (P , 0.05). Insulin receptor substrate (IRS)-1-associated phosphatidylinositol 3-kinase (PI 3K) activity was significantly decreased in PCOS (n = 12) compared with control skeletal muscle (n = 8; P , 0.05). There was no significant difference in the abundance of IR, IRS-1, or the p85 regulatory subunit of PI 3K in PCOS (n = 14) ...
Immunobiological consequence of regulation of insulin receptor on alloactivated lymphocytes in normal and obese subjects<...Immunobiological consequence of regulation of insulin receptor on alloactivated lymphocytes in normal and obese subjects<...
TY - JOUR. T1 - Immunobiological consequence of regulation of insulin receptor on alloactivated lymphocytes in normal and obese subjects. AU - Koffler, Michael. AU - Raskin, Philip. AU - Womble, Debra. AU - Helderman, J. Harold. PY - 1991/1/1. Y1 - 1991/1/1. N2 - Acute manipulations of insulin in vivo regulate the display of insulin receptors induced on activated T lymphocytes after presentation of alloantigen. This study explored the immunobiological consequences of regulation of insulin-receptor display by acute manipulations of insulin achieved during the hyperinsulinemic-euglycemic clamp in healthy normal individuals and obese subjects. T lymphocytes were isolated at 0, 1, and 4 h of hyperinsulinemia from seven normal volunteers and seven obese individuals and studied for their capacity to 1) synthesize a complement of insulin receptors on cell membrane, 2) respond to alloantigen in the mixed-lymphocyte culture (an immunologic activity unrelated to manipulations in insulin concentrations in ...
Trends in prescribing pattern of insulin preparations among uncontrolled type 2 diabetes mellitus patients | International...Trends in prescribing pattern of insulin preparations among uncontrolled type 2 diabetes mellitus patients | International...
Background: Type 2 diabetes mellitus (T2DM) is a progressive disorder of β-cell dysfunction until majority of patients with a longer duration of diabetes remain poorly controlled with oral agents, and use of insulin, which could improve glycemic control .Guidelines from the American Diabetes Association and the European Association for the Study of Diabetes recommend that insulin secretagogues such as sulfonylureas be discontinued at the time of insulin initiation to reduce the risk of hypoglycemia, and that treatment be intensified if HbA1c levels remain above-target 3 months after insulin initiation. Study design and methods: It was a prospective study and patients diagnosed with T2DM initiating insulin and no prior insulin use. The study duration was six months (December 2016 to May 2017) among type 2 diabetes mellitus patients at Karuna Medical College and Hospital, Diabetic centre, Quality clinic-Palakkad. Result and Discussion: Out of total 308 study populations, 226(73.37%) were taking ...
Do low glycemic index diets increase insulin sensitivity in overweight or obese patients?<...Do low glycemic index diets increase insulin sensitivity in overweight or obese patients?<...
TY - JOUR. T1 - Do low glycemic index diets increase insulin sensitivity in overweight or obese patients?. AU - Jana, Kyu. PY - 2016/12/1. Y1 - 2016/12/1. N2 - Among overweight or obese patients without diabetes mellitus, lower glycemic index (GI) diets alone do not improve insulin sensitivity. However, low GI diets combined with high-intensity exercise do improve insulin sensitivity (SOR: C, trials using disease-oriented outcomes).. AB - Among overweight or obese patients without diabetes mellitus, lower glycemic index (GI) diets alone do not improve insulin sensitivity. However, low GI diets combined with high-intensity exercise do improve insulin sensitivity (SOR: C, trials using disease-oriented outcomes).. UR - http://www.scopus.com/inward/record.url?scp=85050716267&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=85050716267&partnerID=8YFLogxK. M3 - Article. AN - SCOPUS:85050716267. VL - 19. SP - E12. JO - Evidence-Based Practice. JF - Evidence-Based Practice. SN - ...
Insulin Glulisine in Adult Subjects With Type 2 Diabetes Receiving Insulin Glargine as Basal Insulin - Full Text View -...Insulin Glulisine in Adult Subjects With Type 2 Diabetes Receiving Insulin Glargine as Basal Insulin - Full Text View -...
The purpose of this study is to compare the change in glycemic control, as measured by hemoglobin A1c (HbA1c) from baseline to study week 24, in subjects receiving insulin glulisine as mealtime insulin following a variable bolus insulin regimen (based on carbohydrate counting) versus a fixed bolus insulin regimen, with insulin glargine as basal insulin in both arms of the study ...
Repositorio da Producao Cientifica e Intelectual da Unicamp: Diurnal variations in insulin secretion and K+ permeability in...Repositorio da Producao Cientifica e Intelectual da Unicamp: Diurnal variations in insulin secretion and K+ permeability in...
1. The effects of glucose on insulin secretion and Rb-86 efflux from isolated rat islets were studied at six different times during a 24-h period (00.00, 04.00, 08.00, 12.00, 16.00 and 20.00 h), 2. In the absence of glucose and in the presence of substimulatory concentrations (2.8 mmol/L) of the sugar, insulin secretion did not vary with the time of day. At a glucose concentration of 5.6 mmol/L the stimulated insulin secretion was greater than basal levels only at 20.00 h, 3. At a higher sugar concentration (8.3 mmol/L) the increase in insulin secretion and the reduction in Rb-86 efflux rate were more marked during the dark period. No effect of the time of day on insulin secretion was observed at glucose concentrations above 8.3 mmol/L (except in 27.7 mmol/L), 4. The time of day appears to affect insulin secretion mainly at glucose concentrations close to physiological values (5.6-8.3 mmol/L), 5. This result agrees with the ability of physiological amounts of glucose to alter the ...
Mechanisms of liver and muscle insulin resistance induced by chronic high-fat feeding | Garvan Institute of Medical ResearchMechanisms of liver and muscle insulin resistance induced by chronic high-fat feeding | Garvan Institute of Medical Research
To elucidate cellular mechanisms of insulin resistance induced by excess dietary fat, we studied conscious chronically high-fat-fed (HFF) and control chow diet-fed rats during euglycemic-hyperinsulinemic (560 pmol/l plasma insulin) clamps. Compared with chow diet feeding, fat feeding significantly impaired insulin action (reduced whole body glucose disposal rate, reduced skeletal muscle glucose metabolism, and decreased insulin suppressibility of hepatic glucose production [HGP]). In HFF rats, hyperinsulinemia significantly suppressed circulating free fatty acids but not the intracellular availability of fatty acid in skeletal muscle (long chain fatty acyl-CoA esters remained at 230% above control levels). In HFF animals, acute blockade of beta-oxidation using etomoxir increased insulin-stimulated muscle glucose uptake, via a selective increase in the component directed to glycolysis, but did not reverse the defect in net glycogen synthesis or glycogen synthase. In clamp HFF animals, etomoxir did not
Relationships between fasting plasma glucose levels and insulin secretion during intravenous glucose tolerance testsRelationships between fasting plasma glucose levels and insulin secretion during intravenous glucose tolerance tests
Insulin secretion and glucose disappearance rate were measured in 66 subjects with a wide range of fasting plasma glucose levels. The acute insulin response was present in subjects with fasting glucose levels below 115 mg/dl but was absent above this level. The glucose disappearance rate related to …
Nutrients | Free Full-Text | Insulin Sensitivity and Glucose Homeostasis Can Be Influenced by Metabolic Acid Load | HTMLNutrients | Free Full-Text | Insulin Sensitivity and Glucose Homeostasis Can Be Influenced by Metabolic Acid Load | HTML
Recent epidemiological findings suggest that high levels of dietary acid load can affect insulin sensitivity and glucose metabolism. Consumption of high protein diets results in the over-production of metabolic acids which has been associated with the development of chronic metabolic disturbances. Mild metabolic acidosis has been shown to impair peripheral insulin action and several epidemiological findings suggest that metabolic acid load markers are associated with insulin resistance and impaired glycemic control through an interference intracellular insulin signaling pathways and translocation. In addition, higher incidence of diabetes, insulin resistance, or impaired glucose control have been found in subjects with elevated metabolic acid load markers. Hence, lowering dietary acid load may be relevant for improving glucose homeostasis and prevention of type 2 diabetes development on a long-term basis. However, limitations related to patient acid load estimation, nutritional determinants, and
Associations of age with serum insulin, proinsulin and the proinsulin-to-insulin ratio: a cross-sectional study | BMC Endocrine...Associations of age with serum insulin, proinsulin and the proinsulin-to-insulin ratio: a cross-sectional study | BMC Endocrine...
Insulin responses and insulin levels seem to decline with age. However, the question of beta cell impairment attributable to ageing has been sparsely addressed in population-based studies. Non-fasting insulin levels are determined by the ambient degree of insulin resistance together with the capacity of beta cells to compensate by insulin secretion to prevent hyperglycaemia. A raised proinsulin-to-insulin ratio (proinsulin/insulin) due to impaired processing of proinsulin is an early marker of beta cell dysfunction. We hypothesised that in a general population, signs of beta cell failure with advancing age manifest not only by decreases in random insulin, but also with a corresponding increase in its precursor proinsulin. In the Tromsø Study 1994-95 we measured insulin and proinsulin concentrations in random blood samples from 6212 persons without self-reported diabetes mellitus and plotted the levels as percentiles according to age. In regression analyses we assessed the relationships between age and
Largest Study To Date Finds Insulin Pumps Result In Better Blood Sugar Control Than Multiple Daily Injections In People With...Largest Study To Date Finds Insulin Pumps Result In Better Blood Sugar Control Than Multiple Daily Injections In People With...
The Lancet. Insulin pumps are significantly more effective at controlling blood glucose (sugar) in people with type 2 diabetes who have failed to respond to the usual standard of care, multiple daily insulin injections, according to the largest international study to examine the safety and effectiveness of the pumps to treat type 2 diabetes, published in The Lancet.. Type 2 diabetes is usually controlled by diet and medication, but most people with advanced disease also end up needing insulin therapy to achieve control of their blood sugar. However, roughly a third of these patients struggle to achieve the right level of blood sugar control with insulin injections many times a day. The growing obesity epidemic is adding to the problem by leading to greater insulin resistance.. Insulin pumps are portable devices attached to the body which deliver constant amounts of rapid or short acting insulin via a catheter placed under the skin. Previous randomised trials comparing the efficacy of insulin ...
PVHL is a regulator of glucose metabolism and insulin secretion in pancreatic beta cells. - Radcliffe Department of MedicinePVHL is a regulator of glucose metabolism and insulin secretion in pancreatic beta cells. - Radcliffe Department of Medicine
Insulin secretion from pancreatic beta cells is stimulated by glucose metabolism. However, the relative importance of metabolizing glucose via mitochondrial oxidative phosphorylation versus glycolysis for insulin secretion remains unclear. von Hippel-Lindau (VHL) tumor suppressor protein, pVHL, negatively regulates hypoxia-inducible factor HIF1alpha, a transcription factor implicated in promoting a glycolytic form of metabolism. Here we report a central role for the pVHL-HIF1alpha pathway in the control of beta-cell glucose utilization, insulin secretion, and glucose homeostasis. Conditional inactivation of Vhlh in beta cells promoted a diversion of glucose away from mitochondria into lactate production, causing cells to produce high levels of glycolytically derived ATP and to secrete elevated levels of insulin at low glucose concentrations. Vhlh-deficient mice exhibited diminished glucose-stimulated changes in cytoplasmic Ca(2+) concentration, electrical activity, and insulin secretion, which culminate
Pre-Mixed Insulin :: Diabetes Education OnlinePre-Mixed Insulin :: Diabetes Education Online
The benefit of pre-mixed insulin is that the fast- and long-acting insulin is combined. No mixing of the insulin is necessary, and there is only one injection.. The disadvantage is that NPH, which has a relatively unpredictable action, is the only long-acting insulin that can be used. Also, when the doses in a mixture is increased or decreased, the amount both of the short acting insulin and long-acting insulin changes, which increases the risk of both high and low blood sugars. Mixtures also dont allow a separate correction to be made for high blood sugars.. (You may wonder why there are NO pre-mixed insulins using Lantus and detemir. This is because insulin glargine (Lantus®) and detemir (Levemir®) cannot be mixed in the same syringe with other insulins!). Pre-mixed insulins are usually prescribed for patients needing a simple insulin treatment plan, and sliding scale therapy.. ...
Hyperlipid: Metformin (05) Insulin ResistanceHyperlipid: Metformin (05) Insulin Resistance
The initial conclusion here was that metformin only facilitates blood glucose reduction in the presence of insulin. Metformin should, theoretically, blunt the action of insulin. But if we consider that at high levels of insulin the function of that insulin is to limit its own action, I think it would be much better viewed as metformin blunts insulin induced insulin resistance. Insulin was bolused iv at 90 minutes. It will have given a massively supra-physiological plasma level. Insulin induced insulin resistance in the insulin treated group appears to be absent at 30 minutes (ie 120 minutes on the graph), to have started at 60 minutes (150 minutes on the graph) and to have gotten p to below 0.05 at 90 minutes (180 minutes on the graph). Of course under an-insulinaemic conditions there is no insulin signalling to facilitate or block, hence the zero to 90 minutes on the graph where metformin has no effect on blood glucose before insulin was bolused ...
Sex differences in insulin resistance in GABAB1 knockout mice - edocSex differences in insulin resistance in GABAB1 knockout mice - edoc
We have previously demonstrated that the absence of functional GABA B receptors (GABABRs) disturbs glucose homeostasis in GABAB1KO mice. The aim of this work was to extend our studies of these alterations in GABAB1KO mice and investigate the sexual differences therein.; Male and female, GABAB1KO and WT mice were used. Glucose and insulin tolerance tests (GTT and ITT), and insulin and glucagon secretion tests (IST and GST) were performed. Blood glucose, serum insulin and hyperglycemic hormones were determined, and HOMA-IR calculated. Skeletal muscle insulin receptor β subunit (IRβ), insulin receptor substrates 1/2 (IRS1, IRS2) and hexokinase-II levels were determined by Western blot. Skeletal muscle insulin sensitivity was assessed by in vivo insulin-induced Akt phosphorylation (Western blot). Food intake and hypothalamic NPY mRNA expression (by qPCR) were also evaluated.; Fasted insulin and HOMA-IR were augmented in GABAB1KO males, with no alterations in females. Areas under the curve (AUC) ...
Identification of fatty acid binding protein 4 as an adipokine that regulates insulin secretion during obesity - Department of...Identification of fatty acid binding protein 4 as an adipokine that regulates insulin secretion during obesity - Department of...
A critical feature of obesity is enhanced insulin secretion from pancreatic β-cells, enabling the majority of individuals to maintain glycaemic control despite adiposity and insulin resistance. Surprisingly, the factors coordinating this adaptive β-cell response with adiposity have not been delineated. Here we show that fatty acid binding protein 4 (FABP4/aP2) is an adipokine released from adipocytes under obesogenic conditions, such as hypoxia, to augment insulin secretion. The insulinotropic action of FABP4 was identified using an invitro system that recapitulates adipocyte to β-cell endocrine signalling, with glucose-stimulated insulin secretion (GSIS) as a functional readout, coupled with quantitative proteomics. Exogenous FABP4 potentiated GSIS invitro and invivo, and circulating FABP4 levels correlated with GSIS in humans. Insulin inhibited FABP4 release from adipocytes invitro, in mice and in humans, consistent with feedback regulation. These data suggest that FABP4 and insulin form an
JCI - Influence of hyperglycemia on insulins in vivo effects in type II diabetes.JCI - Influence of hyperglycemia on insulin's in vivo effects in type II diabetes.
The present study was designed to quantitate the interaction between the decrease in target tissue insulin action seen in subjects with Type II diabetes and the mass action effect of glucose exerted via the prevailing hyperglycemic state. To this end, euglycemic glucose clamp studies were performed in 26 control subjects using insulin infusion rates of 15, 40, 120, 240, and 1,200 mU/M2 per min and in 10 Type II diabetic subjects using insulin infusion rates of 120 and 1,200 mU/M2 per min. The results of these euglycemic studies indicated that insulin-stimulated peripheral glucose disposal was decreased in the Type II diabetics due to a combined receptor (rightward shift in the dose-response curve) and postreceptor defect in insulin action (decreased maximal response), whereas the decrease in insulin-mediated suppression of hepatic glucose output (HGO) was consistent with a defect in insulin binding (rightward shift in dose-response curve). Hyperglycemic glucose clamp studies were also performed ...
Insulin Action in Rats Is Influenced by Amount and Composition of Dietary FatInsulin Action in Rats Is Influenced by Amount and Composition of Dietary Fat
The chronic influence of dietary fat composition on obesity and insulin action is not well understood. We examined the effect of amount (20% vs 60% of total calories) and type (saturated vs polyunsaturated) of fat on insulin action and body composition in mature male rats. Six months of feeding a high fat (HF) diet led to obesity and impaired insulin action (determined by a euglycemic‐hyperinsulinemic clamp), neither of which were reversed by a subsequent 6 months of feeding a low fat (LF) diet. Within HF fed rats, type of fat did not affect body composition or insulin action. Six months of feeding a low fat diet led to only a slight decline in insulin action, with no difference due to type of dietary fat. From 6-9 months, insulin action became more impaired in LF rats fed the saturated diet than in LF rats fed the polyunsaturated diet. By 12 months, all groups were obese and had a similar impairment in insulin action. The amount and type of fat in the diet did not influence the overall degree ...
DynaMed Weekly Update 19 - Combination of Metformin plus Insulin May Not Reduce Mortality Compared to Insulin Alone in Patients...DynaMed Weekly Update 19 - Combination of Metformin plus Insulin May Not Reduce Mortality Compared to Insulin Alone in Patients...
Combination of Metformin plus Insulin May Not Reduce Mortality Compared to Insulin Alone in Patients with Type 2 Diabetes. For patients with type 2 diabetes mellitus inadequately treated with lifestyle modifications and oral antidiabetic agents, combined use of metformin and insulin is recommended by the American Diabetes Association and the European Association for the Study of Diabetes as part of a consensus treatment algorithm (Diabetologia 2009 Jan;52(1):17). A new systematic review of 26 randomized trials compared the effects of combination therapy vs. insulin alone on clinical outcomes in 2,286 patients with type 2 diabetes. Trial durations ranged from 3 months to 4.3 years, with a median duration of 6 months. Most of the trials had some methodologic limitations including incomplete blinding, baseline differences between randomized groups, and unclear allocation concealment. In meta-analyses, there were no significant differences in all-cause mortality (risk ratio 1.3, 95% CI 0.57-2.99) or ...
Neural top-down control of physiologyNeural top-down control of physiology
Donald HarveyDonald Harvey
Congenital generalized lipodystrophyCongenital generalized lipodystrophy
Karin M. HehenbergerKarin M. Hehenberger
Glycemic indexGlycemic index
Rejuvenation (aging)Rejuvenation (aging)
Medical Technology GroupMedical Technology Group
John Jacob AbelJohn Jacob Abel
Bigfoot BiomedicalBigfoot Biomedical
Subcutaneous injectionSubcutaneous injection
PIKFYVEPIKFYVE
Glossary of diabetesGlossary of diabetes
Daya Kishore HazraDaya Kishore Hazra
Frederic M. RichardsFrederic M. Richards
Signal transductionSignal transduction
Accessible surface areaAccessible surface area
History of genetic engineeringHistory of genetic engineering
Heart failure with preserved ejection fractionHeart failure with preserved ejection fraction
Health in MaliHealth in Mali
List of unproven and disproven cancer treatmentsList of unproven and disproven cancer treatments
Bolus (medicine)Bolus (medicine)
Banting HouseBanting House
Phosphatidylinositol 5-phosphatePhosphatidylinositol 5-phosphate
Protein structureProtein structure
Familial partial lipodystrophyFamilial partial lipodystrophy
Pharmaceutical industryPharmaceutical industry
Glucose meterGlucose meter
Downregulation and upregulationDownregulation and upregulation
Schulich School of Medicine & DentistrySchulich School of Medicine & Dentistry
Mark Atkinson (scientist)Mark Atkinson (scientist)
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPsychiatry and PsychologyPhenomena and ProcessesTechnology, Industry, AgricultureInformation ScienceHealth Care
InsulinReceptor, InsulinInsulin ResistanceInsulin Receptor Substrate ProteinsGlucoseInsulin, Long-ActingInsulin AntibodiesHypoglycemic AgentsInsulin AntagonistsIslets of LangerhansInsulin LisproGlucose Tolerance TestDiabetes Mellitus, Type 2Insulin Infusion SystemsGlucose Clamp TechniqueInsulin AspartInsulin, IsophaneInsulin, Regular, PorkHyperinsulinismAdipose TissueInsulin-Secreting CellsInsulinsGlucagonObesityInsulin, Regular, HumanC-PeptideProinsulinFastingBlood GlucoseHyperglycemiaLiverMuscle, SkeletalDiabetes Mellitus, Type 1Signal TransductionFatty Acids, NonesterifiedGlucose Transporter Type 4AdipocytesInsulin, Short-ActingHypoglycemiaPhosphorylationDiabetes Mellitus, ExperimentalDiabetes MellitusGlucose IntoleranceInsulin-Like Growth Factor ILeptinDeoxyglucoseBody WeightTriglyceridesPhosphoproteinsMonosaccharide Transport ProteinsPhosphatidylinositol 3-KinasesInsulinomaCells, CulturedBiphasic InsulinsKineticsProto-Oncogene Proteins c-aktHemoglobin A, GlycosylatedGlycogenHomeostasisAdiponectinPostprandial PeriodRats, WistarLipidsTime FactorsPancreasGlucagon-Like Peptide 1Cell LineBody Mass IndexMetforminDietary FatsDose-Response Relationship, DrugMice, ObeseLipid MetabolismRNA, MessengerRats, Inbred StrainsThiazolidinediones3T3-L1 CellsLipolysisMuscle ProteinsRats, Sprague-DawleyReceptor, IGF Type 1Rats, ZuckerMice, Inbred C57BLMetabolic Syndrome XTolbutamideInfusions, SubcutaneousEatingDietary CarbohydratesGene Expression RegulationBody CompositionBiological TransportDiet, High-FatReference ValuesStreptozocinMice, KnockoutEnergy MetabolismGlycogen SynthaseSomatostatinAdiposityGluconeogenesis3-O-MethylglucoseGlucokinaseEnzyme ActivationGrowth HormoneFatty LiverTyrosineInjections, SubcutaneousPolycystic Ovary Syndrome3T3 CellsFatty AcidsProtein-Serine-Threonine KinasesHormonesInsulysinSulfonylurea CompoundsFructoseCell MembraneGastric Inhibitory PolypeptideModels, BiologicalDiabetic KetoacidosisPrediabetic StateProteinsMusclesCricetinaeDietProtein Tyrosine Phosphatase, Non-Receptor Type 1Glucose Transporter Type 2Cross-Over StudiesInfusions, IntravenousMolecular Sequence DataAndrostadienesProtein-Tyrosine KinasesRibosomal Protein S6 KinasesDiazoxideBlotting, WesternEpinephrineGlycerolResistinIntra-Abdominal FatGene ExpressionMethylglucosidesRisk FactorsLeucinePregnancyAdipokinesTransfectionAmino AcidsStimulation, ChemicalVenomsPalmitatesBlood PressureCalciumEnzyme InhibitorsExocytosisReceptors, SomatomedinDisease Models, AnimalBiological MarkersMice, TransgenicCHO CellsAmino Acid SequenceArea Under CurveHydrocortisoneIntracellular Signaling Peptides and ProteinsIslets of Langerhans TransplantationBlood Glucose Self-MonitoringEnergy IntakeGhrelinWeight GainGlucose Transporter Type 1Adenoma, Islet CellPhosphotyrosineOxidation-ReductionPPAR gammaPalmitic AcidDexamethasoneProto-Oncogene ProteinsInsulin ComaPancreas, ArtificialDiabetes, GestationalTranscription FactorsReverse Transcriptase Polymerase Chain ReactionInsulin-Like Growth Factor IICyclic AMPRadioimmunoassayAnalysis of VarianceSwineLactatesGlucose-6-PhosphataseArginineAgingReceptors, GlucagonWeight Loss3-Hydroxybutyric AcidPerfusionSecretory RateLactic AcidInflammationAdipose Tissue, WhiteAdenosine TriphosphateGlycolysisProtein KinasesRecombinant Proteins
Lemon detox diet reduced body fat, insulin resistance, and serum hs-CRP level without hematological changes in overweight...Lemon detox diet reduced body fat, insulin resistance, and serum hs-CRP level without hematological changes in overweight...
9 Proven Ways to Fix The Hormones That Control Your Weight9 Proven Ways to Fix The Hormones That Control Your Weight
Insulin pump - WikipediaInsulin pump - Wikipedia
insulin | PNASinsulin | PNAS
Insulin Therapy | MedscapeInsulin Therapy | Medscape
insulin | PBS NewsHourinsulin | PBS NewsHour
Blood Test: InsulinBlood Test: Insulin
Word! Insulin ResistanceWord! Insulin Resistance
Insulin Basics | ADAInsulin Basics | ADA
Insulin Basics | ADAInsulin Basics | ADA
Types of Insulin | Diabetes | CDCTypes of Insulin | Diabetes | CDC
Insulin Resistance and Diabetes | CDCInsulin Resistance and Diabetes | CDC
Where are all the generic insulins hiding?Where are all the generic insulins hiding?
Human insulin | The BMJHuman insulin | The BMJ
Insulin: Function and typesInsulin: Function and types
Human insulin. | The BMJHuman insulin. | The BMJ
Insulin DiseasesInsulin Diseases
Insulin-like growth factor 2 - WikipediaInsulin-like growth factor 2 - Wikipedia
Lillys Lower-Priced Insulin Now AvailableLilly's Lower-Priced Insulin Now Available
How is insulin resistance assessed?How is insulin resistance assessed?
Does insulin make you faster?Does insulin make you faster?
Insulin pumps: MedlinePlus Medical EncyclopediaInsulin pumps: MedlinePlus Medical Encyclopedia
Insulin isolated in Toronto - HISTORYInsulin isolated in Toronto - HISTORY
Insulin Resistance TreatmentInsulin Resistance Treatment
Administering Insulin - JDRFAdministering Insulin - JDRF
Insulin | Buzzle.comInsulin | Buzzle.com
Apidra (insulin glulisine)Apidra (insulin glulisine)
Insulin Treatment | HealthCentralInsulin Treatment | HealthCentral
U.S. regulator approves Afrezza inhalable insulinU.S. regulator approves Afrezza inhalable insulin
The Mode of Action of Insulin | NatureThe Mode of Action of Insulin | Nature
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPsychiatry and PsychologyPhenomena and ProcessesTechnology, Industry, AgricultureInformation ScienceHealth Care
InsulinReceptor, InsulinInsulin ResistanceInsulin Receptor Substrate ProteinsGlucoseInsulin, Long-ActingInsulin AntibodiesHypoglycemic AgentsInsulin AntagonistsIslets of LangerhansInsulin LisproGlucose Tolerance TestDiabetes Mellitus, Type 2Insulin Infusion SystemsGlucose Clamp TechniqueInsulin AspartInsulin, IsophaneInsulin, Regular, PorkHyperinsulinismAdipose TissueInsulin-Secreting CellsInsulinsGlucagonObesityInsulin, Regular, HumanC-PeptideProinsulinFastingBlood GlucoseHyperglycemiaLiverMuscle, SkeletalDiabetes Mellitus, Type 1Signal TransductionFatty Acids, NonesterifiedGlucose Transporter Type 4AdipocytesInsulin, Short-ActingHypoglycemiaPhosphorylationDiabetes Mellitus, ExperimentalDiabetes MellitusGlucose IntoleranceInsulin-Like Growth Factor ILeptinDeoxyglucoseBody WeightTriglyceridesPhosphoproteinsMonosaccharide Transport ProteinsPhosphatidylinositol 3-KinasesInsulinomaCells, CulturedBiphasic InsulinsKineticsProto-Oncogene Proteins c-aktHemoglobin A, GlycosylatedGlycogenHomeostasisAdiponectinPostprandial PeriodRats, WistarLipidsTime FactorsPancreasGlucagon-Like Peptide 1Cell LineBody Mass IndexMetforminDietary FatsDose-Response Relationship, DrugMice, ObeseLipid MetabolismRNA, MessengerRats, Inbred StrainsThiazolidinediones3T3-L1 CellsLipolysisMuscle ProteinsRats, Sprague-DawleyReceptor, IGF Type 1Rats, ZuckerMice, Inbred C57BLMetabolic Syndrome XTolbutamideInfusions, SubcutaneousEatingDietary CarbohydratesGene Expression RegulationBody CompositionBiological TransportDiet, High-FatReference ValuesStreptozocinMice, KnockoutEnergy MetabolismGlycogen SynthaseSomatostatinAdiposityGluconeogenesis3-O-MethylglucoseGlucokinaseEnzyme ActivationGrowth HormoneFatty LiverTyrosineInjections, SubcutaneousPolycystic Ovary Syndrome3T3 CellsFatty AcidsProtein-Serine-Threonine KinasesHormonesInsulysinSulfonylurea CompoundsFructoseCell MembraneGastric Inhibitory PolypeptideModels, BiologicalDiabetic KetoacidosisPrediabetic StateProteinsMusclesCricetinaeDietProtein Tyrosine Phosphatase, Non-Receptor Type 1Glucose Transporter Type 2Cross-Over StudiesInfusions, IntravenousMolecular Sequence DataAndrostadienesProtein-Tyrosine KinasesRibosomal Protein S6 KinasesDiazoxideBlotting, WesternEpinephrineGlycerolResistinIntra-Abdominal FatGene ExpressionMethylglucosidesRisk FactorsLeucinePregnancyAdipokinesTransfectionAmino AcidsStimulation, ChemicalVenomsPalmitatesBlood PressureCalciumEnzyme InhibitorsExocytosisReceptors, SomatomedinDisease Models, AnimalBiological MarkersMice, TransgenicCHO CellsAmino Acid SequenceArea Under CurveHydrocortisoneIntracellular Signaling Peptides and ProteinsIslets of Langerhans TransplantationBlood Glucose Self-MonitoringEnergy IntakeGhrelinWeight GainGlucose Transporter Type 1Adenoma, Islet CellPhosphotyrosineOxidation-ReductionPPAR gammaPalmitic AcidDexamethasoneProto-Oncogene ProteinsInsulin ComaPancreas, ArtificialDiabetes, GestationalTranscription FactorsReverse Transcriptase Polymerase Chain ReactionInsulin-Like Growth Factor IICyclic AMPRadioimmunoassayAnalysis of VarianceSwineLactatesGlucose-6-PhosphataseArginineAgingReceptors, GlucagonWeight Loss3-Hydroxybutyric AcidPerfusionSecretory RateLactic AcidInflammationAdipose Tissue, WhiteAdenosine TriphosphateGlycolysisProtein KinasesRecombinant Proteins
SyringesSyringeAmount of insulinCalled insulin resistanceGlucose2020ResistanceLong-actingSensitivitySecretionInjectionBolusTypes of insulinUnits of insulinEffects of insulinDiabeticTake insulinEnough insulinHormoneReceptorAbsorptionHypoglycemiaNEEDLESProteinsPeople with diabetesOmniPodBasal insulinInject insulinPumping InsulinMetabolismFast actingPancreas releasesPumpsVialNovo NordiskLillyDeliver InsulinForm of insulinLevel of insulinDoses of insulinLevels of insulinKeep your insulinRelease of insulinControl of insulinDoseNeedleNovoLogHormonesPorcinePensLess insulinMake insulinHuman insulinDiabetes SuppliesMealsCarbsAntibodiesReceptorsTypeReservoirCartridgesMeal
Syringes1
Syringe11
Amount of insulin7
Called insulin resistance2
Glucose21
20202
Resistance22
Long-acting2
Sensitivity19
Secretion3
Injection5
Bolus3
  • Also it looks like Allie has already answered the question, but I'll add that any bolus you give that is not a correction and is not for carbs (for example hit "bolus" from home screen, then hit "no" to BG and hit "no" to carbs, and you can still dial up units of insulin and confirm that for a bolus) will also NOT be counted in IOB. (tudiabetes.org)
  • This is contrasted to mealtime, or bolus, insulin which has a rapid onset and is typically used to control blood sugar levels during meals. (buyinsulin.com)
  • An extended meal bolus delivers insulin over a longer period of time. (omnipod.com)
Types of insulin4
Units of insulin3
Effects of insulin3
Diabetic2
  • I'm a diabetic in good control despite myself - I don't check my blood sugar as often as i should, since my insurance refused my insulin pen, I don't even do my insulin as often as i'm supposed to. (livejournal.com)
  • As a type 1 diabetic himself, who was also in need of affordable insulin, Worth decided to bring his camera on the trip. (monmouthfilmfestival.org)
Take insulin2
Enough insulin2
Hormone14
Receptor3
Absorption4
Hypoglycemia2
NEEDLES3
Proteins6
  • However, many critical questions are still unclear regarding insulin activation, and the activation process of the other insulin -family proteins, namely insulin - like growth factor I (IGF-I) and II (IGF-II). (oatd.org)
  • Deficiency of these proteins can lead to chronic diseases, with insulin being involved in diabetes and IGFs in cancer. (oatd.org)
  • We have examined the effects of combinations of insulin and the counterregulatory hormones (dexamethasone, glucagon, and epinephrine), in the presence or absence of interleukin (IL)-6, on the production by isolated hepatocytes of the positive acute-phase proteins C-reactive protein, alpha 1-antichymotrypsin, alpha 1-acid glycoprotein, and haptoglobin, and the negative acute-phase proteins prealbumin and transferrin. (ed.ac.uk)
  • The effect of IL-6 on the production of the above proteins was influenced significantly by insulin and all of the counterregulatory hormones. (ed.ac.uk)
  • The results indicate that both positive and negative acute-phase proteins respond differently to insulin and the counterregulatory hormones and that the potential exists for the regulation of synthesis of individual acute-phase reactants by interaction between the cytokine network and the classical endocrine hormones. (ed.ac.uk)
  • Other buy Insulin in Canada proteins are enzymes that cause chemical reactions within the body, and some proteins can be used for energy. (sweetchicknyc.com)
People with diabetes3
  • And there are 3.5 million people [with diabetes, some of whom] rely on insulin, not least the Prime Minister. (diabetesdietblog.com)
  • I hope all the people with diabetes mellitus in the UK can get insulin when they need it after the UK exits the European Union. (diabetesdietblog.com)
  • Simple, nonstop insulin delivery for people with diabetes who insist life still comes first. (omnipod.com)
OmniPod2
  • A few tubing-free "patch" pumps, such as the OmniPod, stick to the body and direct insulin through a cannula inserted into the skin beneath the device. (diabetesforecast.org)
  • This resource guide will lead you through some of the key functions you may need to perform with the Omnipod ® Insulin Management System. (omnipod.com)
Basal insulin1
  • These devices are programmed to deliver a small continuous flow of rapid-acting insulin around the clock-basal insulin-as well as on-demand doses selected by the user to cover carbohydrate in meals, snacks, and beverages. (diabetesforecast.org)
Inject insulin1
Pumping Insulin2
  • Between the two face-to-face appointments and the daily follow up calls after I started pumping insulin, I feel like I've given them enough of an opportunity to prove themselves. (tobesugarfree.com)
  • It is a rule of thumb based on the work of John Walsh (Author of Pumping Insulin ). (blogspot.com)
Metabolism1
Fast acting1
Pancreas releases1
Pumps6
Vial2
  • changed out the reservoir to a different lot, changed infusion set to different lot, changed out the battery, tried new vial of insulin, but still air bubbles. (tudiabetes.org)
  • The acts of inverting the insulin vial and drawing insulin into the cartridge will create air bubbles that are too small for the eye to see. (tudiabetes.org)
Novo Nordisk2
  • In hopes of coming up with an alternative to those injections, MIT engineers, working with scientists from Novo Nordisk, have designed a new drug capsule that can carry insulin or other protein drugs and protect them from the harsh environment of the gastrointestinal tract. (technics-goods.info)
  • But when Novo Nordisk entered the market four years later with its personal analog insulin, NovoLog, costs did not lower on account of competition. (uaz-buhanka.ru)
Lilly1
Deliver Insulin1
  • In most cases, they deliver insulin through an infusion set: tubing that winds from the pump to a needle or cannula-a tiny flexible tube-inserted under the skin. (diabetesforecast.org)
Form of insulin2
  • INSULIN ASPART (IN su lin AS part) is a human-made form of insulin. (umassmemorial.org)
  • The venom of cone snails contains a unique form of insulin which works much faster than human insulin. (eara.eu)
Level of insulin1
Doses of insulin1
Levels of insulin2
  • We can only minimize levels of insulin (the fat blocker) by decreasing our carb intake. (16-hrs.com)
  • There is also some evidence that these raised levels of insulin are one of the big drivers of obesity. (thelivingwellgp.co.uk)
Keep your insulin2
  • For instance, choose a spot to keep your insulin and meter, and make sure you put them there each and every night, so you know right where they are when you need them in the morning. (tycoonpress.com)
  • The wallets let you keep your insulin pen cool in warm temperatures. (diabetesplan.org)
Release of insulin2
  • It supplies a steady release of insulin to help control your blood sugar levels overnight and between meals. (buyinsulin.com)
  • This means there is also a constant release of insulin which has a number of effects on the body. (thelivingwellgp.co.uk)
Control of insulin2
  • The control of insulin is central to what I profess at 16-hrs For Life. (16-hrs.com)
  • The liver does this really efficiently under the control of insulin but has only a limited capacity to store glycogen. (thelivingwellgp.co.uk)
Dose7
Needle3
  • Earlier this year, they developed a blueberry-sized capsule containing a small needle made of compressed insulin. (technics-goods.info)
  • I pushed the plunger down as normal, but when I took the needle out a few drops on insulin spilled out onto the floor. (mrbump.uk)
  • The human-robot teams insert the empty insulin bags into their plastic cases and seal the bag with lasers, leaving only a one-way plug that the user pierces with a needle to fill the bag with insulin. (diabetesforecast.org)
NovoLog1
  • Novolog Vials: Store in a refrigerator between 2 and 8 degrees C (36 and 46 degrees F) or at room temperature below 30 degrees C (86 degrees F). Do not freeze or use if the insulin has been frozen. (umassmemorial.org)
Hormones4
  • Like all hormones, insulin has important functions, and an optimal level. (diabetestalk.net)
  • Insulin and counterregulatory hormones influence acute-phase protein p. (ed.ac.uk)
  • Significant three-way interactions as well as higher order interactions between the stress hormones and insulin were seen in the case of C-reactive protein. (ed.ac.uk)
  • Insulin also has been found to inhibit other hormones related to satiety, the signals that tell the brain that you are full and to stop you eating more. (thelivingwellgp.co.uk)
Porcine2
Pens6
  • There are two basic types of pens: disposable pens, which are preloaded with insulin and tossed out after the insulin runs out, and reusable pens, which are loaded by the user and can be refilled with cartridges that are purchased separately. (diabetesforecast.org)
  • I use it several times (about 2 pens per week), using a little bit more of the insulin each time. (mrbump.uk)
  • Disposable insulin pens are refrigerated before use and then may be kept at room temperature once you start to use. (diabetesplan.org)
  • Reusable insulin pens have replacement cartridges that are reloaded with a new insulin cartridge. (diabetesplan.org)
  • Insulin pens typically come in two types, pre-filled and durable. (wisegeek.net)
  • Durable insulin pens have replaceable insulin cartridges, while pre-filled pens can be completely discarded when the insulin cartridge is empty. (wisegeek.net)
Less insulin2
Make insulin1
Human insulin3
  • To introduce this fast-acting quality to human insulin the group identified key amino acids for the function of snail insulin and integrated modified versions of them into an adapted human insulin molecule. (eara.eu)
  • When tested in rats , this hybrid insulin molecule had the same potency as human insulin while acting faster. (eara.eu)
  • Lantus works by controlling blood sugar levels in the body just like naturally occurring human insulin does. (buyinsulin.com)
Diabetes Supplies3
  • Insulin For Life is a not-for profit organisation that collects insulin and other diabetes supplies that would otherwise be wasted, to be redistributed to countries who cannot afford it or places affected by natural disasters. (bittersweetdiagnosis.com)
  • While some Young Leaders have had first hand experiences with limited access to insulin or diabetes supplies, we are all well aware of the consequences. (bittersweetdiagnosis.com)
  • We obtain insulin and other diabetes supplies to donate to diabetes associations and other responsible organisations in countries in need. (insulinforlife.org.au)
Meals4
Carbs1
  • The pod does not consider insulin given for carbs as IOB because it's there to counteract the food you ate. (tudiabetes.org)
Antibodies1
  • At times the body may produce auto-antibodies against insulin itself {anti-insulin antibodies} reducing its availability or rendering it less effective or not effective at all. (bdtype1.com)
Receptors6
Type11
Reservoir1
Cartridges1
  • Tandem can currently make 1 million insulin cartridges per year in a single shift at its San Diego headquarters in an assembly line that includes humans wearing clean gowns and boxy robots. (diabetesforecast.org)
Meal2

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