Hyperglycemia. Medical search

Abnormally high BLOOD GLUCOSE level.

Glucose in blood.

Diabetes mellitus induced experimentally by administration of various diabetogenic agents or by PANCREATECTOMY.

A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).

A 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.

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.

Substances which lower blood glucose levels.

An antibiotic that is produced by Stretomyces achromogenes. It is used as an antineoplastic agent and to induce diabetes in experimental animals.

A test to determine the ability of an individual to maintain HOMEOSTASIS of BLOOD GLUCOSE. It includes measuring blood glucose levels in a fasting state, and at prescribed intervals before and after oral glucose intake (75 or 100 g) or intravenous infusion (0.5 g/kg).

A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.

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.

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.

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.

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.

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)

Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.

A type of pancreatic cell representing about 50-80% of the islet cells. Beta cells secrete INSULIN.

Minor hemoglobin components of human erythrocytes designated A1a, A1b, and A1c. Hemoglobin A1c is most important since its sugar moiety is glucose covalently bound to the terminal amino acid of the beta chain. Since normal glycohemoglobin concentrations exclude marked blood glucose fluctuations over the preceding three to four weeks, the concentration of glycosylated hemoglobin A is a more reliable index of the blood sugar average over a long period of time.

The time frame after a meal or FOOD INTAKE.

Abstaining from all food.

Conditions or pathological processes associated with the disease of diabetes mellitus. Due to the impaired control of BLOOD GLUCOSE level in diabetic patients, pathological processes develop in numerous tissues and organs including the EYE, the KIDNEY, the BLOOD VESSELS, and the NERVE TISSUE.

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.

VASCULAR DISEASES that are associated with DIABETES MELLITUS.

The appearance of an abnormally large amount of GLUCOSE in the urine, such as more than 500 mg/day in adults. It can be due to HYPERGLYCEMIA or genetic defects in renal reabsorption (RENAL GLYCOSURIA).

Biosynthesis of GLUCOSE from nonhexose or non-carbohydrate precursors, such as LACTATE; PYRUVATE; ALANINE; and GLYCEROL.

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.

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.

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.

A serious complication of TYPE 2 DIABETES MELLITUS. It is characterized by extreme HYPERGLYCEMIA; DEHYDRATION; serum hyperosmolarity; and depressed consciousness leading to COMA in the absence of KETOSIS and ACIDOSIS.

KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.

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.

The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.

A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.

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.

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.

The state of PREGNANCY in women with DIABETES MELLITUS. This does not include either symptomatic diabetes or GLUCOSE INTOLERANCE induced by pregnancy (DIABETES, GESTATIONAL) which resolves at the end of pregnancy.

Elements of limited time intervals, contributing to particular results or situations.

Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.

A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.

A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).

A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).

A 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.

An autosomal recessive metabolic disorder caused by deficiencies in the mitochondrial GLYCINE cleavage system.

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.

Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as CHOREATIC DISORDERS. Chorea is also a frequent manifestation of BASAL GANGLIA DISEASES.

Products derived from the nonenzymatic reaction of GLUCOSE and PROTEINS in vivo that exhibit a yellow-brown pigmentation and an ability to participate in protein-protein cross-linking. These substances are involved in biological processes relating to protein turnover and it is believed that their excessive accumulation contributes to the chronic complications of DIABETES MELLITUS.

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).

Disease of the RETINA as a complication of DIABETES MELLITUS. It is characterized by the progressive microvascular complications, such as ANEURYSM, interretinal EDEMA, and intraocular PATHOLOGIC NEOVASCULARIZATION.

FATTY ACIDS found in the plasma that are complexed with SERUM ALBUMIN for transport. These fatty acids are not in glycerol ester form.

Peripheral, autonomic, and cranial nerve disorders that are associated with DIABETES MELLITUS. These conditions usually result from diabetic microvascular injury involving small blood vessels that supply nerves (VASA NERVORUM). Relatively common conditions which may be associated with diabetic neuropathy include third nerve palsy (see OCULOMOTOR NERVE DISEASES); MONONEUROPATHY; mononeuropathy multiplex; diabetic amyotrophy; a painful POLYNEUROPATHY; autonomic neuropathy; and thoracoabdominal neuropathy. (From Adams et al., Principles of Neurology, 6th ed, p1325)

A disease or state in which death is possible or imminent.

The transference of pancreatic islets within an individual, between individuals of the same species, or between individuals of different species.

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.

An amino sugar formed when glucose non-enzymatically reacts with the N-terminal amino group of proteins. The fructose moiety is derived from glucose by the "classical" Amadori rearrangement.

Disease having a short and relatively severe course.

Mutant mice exhibiting a marked obesity coupled with overeating, hyperglycemia, hyperinsulinemia, marked insulin resistance, and infertility when in a homozygous state. They may be inbred or hybrid.

The 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.

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.

An inhibitor of ALPHA-GLUCOSIDASES that retards the digestion and absorption of DIETARY CARBOHYDRATES in the SMALL INTESTINE.

The release of GLUCOSE from GLYCOGEN by GLYCOGEN PHOSPHORYLASE (phosphorolysis). The released glucose-1-phosphate is then converted to GLUCOSE-6-PHOSPHATE by PHOSPHOGLUCOMUTASE before entering GLYCOLYSIS. Glycogenolysis is stimulated by GLUCAGON or EPINEPHRINE via the activation of PHOSPHORYLASE KINASE.

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.

Conditions with excess LIPIDS in the blood.

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.

Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.

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.

An enzyme that catalyzes the conversion of D-glucose 6-phosphate and water to D-glucose and orthophosphate. EC 3.1.3.9.

The relationship between the dose of an administered drug and the response of the organism to the drug.

Glycogen stored in the liver. (Dorland, 28th ed)

The processes whereby the internal environment of an organism tends to remain balanced and stable.

2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.

An enzyme that catalyzes reversibly the oxidation of an aldose to an alditol. It possesses broad specificity for many aldoses. EC 1.1.1.21.

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)

A state of unconsciousness as a complication of diabetes mellitus. It occurs in cases of extreme HYPERGLYCEMIA or extreme HYPOGLYCEMIA as a complication of INSULIN therapy.

A pancreatic polypeptide of about 110 amino acids, depending on the species, that is the precursor of insulin. Proinsulin, produced by the PANCREATIC BETA CELLS, is comprised sequentially of the N-terminal B-chain, the proteolytically removable connecting C-peptide, and the C-terminal A-chain. It also contains three disulfide bonds, two between A-chain and B-chain. After cleavage at two locations, insulin and C-peptide are the secreted products. Intact proinsulin with low bioactivity also is secreted in small amounts.

A sodium-glucose transporter that is expressed in the luminal membrane of the PROXIMAL KIDNEY TUBULES.

A type of pancreatic cell representing about 5-20% of the islet cells. Alpha cells secrete GLUCAGON.

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.

Portable or implantable devices for infusion of insulin. Includes open-loop systems which may be patient-operated or controlled by a pre-set program and are designed for constant delivery of small quantities of insulin, increased during food ingestion, and closed-loop systems which deliver quantities of insulin automatically based on an electronic glucose sensor.

A 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)

A polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several research applications.

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.

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.

Salts or esters of LACTIC ACID containing the general formula CH3CHOHCOOR.

Accelerated intimal hyperplasia and increased endogenous inhibitors for NO synthesis in rabbits with alloxan-induced hyperglycaemia. (1/3915)

1. We examined whether endogenous inhibitors of NO synthesis are involved in the augmentation of intimal hyperplasia in rabbits with hyperglycaemia induced by alloxan. 2. Four weeks after the endothelial denudation of carotid artery which had been performed 12 weeks after alloxan, the intimal hyperplasia was greatly augmented with hyperglycaemia. The degree of hyperplasia was assessed using three different parameters of histopathological findings as well as changes in luminal area and intima: media ratio. 3. There were positive and significant correlations between intima:media ratio, plasma glucose, and concentrations of N(G)-monomethyl-L-arginine (L-NMMA) and N(G), N(G)-dimethyl-L-arginine (ADMA) in endothelial cells, that is, the intima:media ratio became greater as plasma glucose and endothelial L-NMMA and ADMA were increased. Furthermore, endothelial L-NMMA and ADMA were increased in proportion to the increase in plasma glucose. 4. In contrast, there were inverse and significant correlations between cyclic GMP production by carotid artery strips with endothelium and plasma glucose, between cyclic GMP production and endothelial L-NMMA and ADMA, and between the intima:media ratio and cyclic GMP production. 5. Exogenously applied L-NMMA and ADMA inhibited cyclic GMP production in a concentration-dependent manner. IC50 values were determined to be 12.1 microM for the former and 26.2 microM for the latter. The cyclic GMP production was abolished after the deliberate removal of endothelium from the artery strips. 6. These results suggest that the augmentation of intimal hyperplasia with hyperglycaemia is closely related to increased accumulation of L-NMMA and ADMA with hyperglycaemia, which would result in an accelerated reduction in NO production/release by endothelial cells. (+info)

Effect of hyperglycemia-hyperinsulinemia on whole body and regional fatty acid metabolism. (2/3915)

The effects of combined hyperglycemia-hyperinsulinemia on whole body, splanchnic, and leg fatty acid metabolism were determined in five volunteers. Catheters were placed in a femoral artery and vein and a hepatic vein. U-13C-labeled fatty acids were infused, once in the basal state and, on a different occasion, during infusion of dextrose (clamp; arterial glucose 8.8 +/- 0.5 mmol/l). Lipids and heparin were infused together with the dextrose to maintain plasma fatty acid concentrations at basal levels. Fatty acid availability in plasma and fatty acid uptake across the splanchnic region and the leg were similar during the basal and clamp experiments. Dextrose infusion decreased fatty acid oxidation by 51.8% (whole body), 47.4% (splanchnic), and 64.3% (leg). Similarly, the percent fatty acid uptake oxidized decreased at the whole body level (53 to 29%), across the splanchnic region (30 to 13%), and in the leg (48 to 22%) during the clamp. We conclude that, in healthy men, combined hyperglycemia-hyperinsulinemia inhibits fatty acid oxidation to a similar extent at the whole body level, across the leg, and across the splanchnic region, even when fatty acid availability is constant. (+info)

Effects of duodenal distension on antropyloroduodenal pressures and perception are modified by hyperglycemia. (3/3915)

Marked hyperglycemia (blood glucose approximately 15 mmol/l) affects gastrointestinal motor function and modulates the perception of gastrointestinal sensations. The aims of this study were to evaluate the effects of mild hyperglycemia on the perception of, and motor responses to, duodenal distension. Paired studies were done in nine healthy volunteers, during euglycemia ( approximately 4 mmol/l) and mild hyperglycemia ( approximately 10 mmol/l), in randomized order, using a crossover design. Antropyloroduodenal pressures were recorded with a manometric, sleeve-side hole assembly, and proximal duodenal distensions were performed with a flaccid bag. Intrabag volumes were increased at 4-ml increments from 12 to 48 ml, each distension lasting for 2.5 min and separated by 10 min. Perception of the distensions and sensations of fullness, nausea, and hunger were evaluated. Perceptions of distension (P < 0.001) and fullness (P < 0.05) were greater and hunger less (P < 0.001) during hyperglycemia compared with euglycemia. Proximal duodenal distension stimulated pyloric tone (P < 0.01), isolated pyloric pressure waves (P < 0.01), and duodenal pressure waves (P < 0.01). Compared with euglycemia, hyperglycemia was associated with increases in pyloric tone (P < 0.001), the frequency (P < 0.05) and amplitude (P < 0.01) of isolated pyloric pressure waves, and the frequency of duodenal pressure waves (P < 0.001) in response to duodenal distension. Duodenal compliance was less (P < 0.05) during hyperglycemia compared with euglycemia, but this did not account for the effects of hyperglycemia on perception. We conclude that both the perception of, and stimulation of pyloric and duodenal pressures by, duodenal distension are increased by mild hyperglycemia. These observations are consistent with the concept that the blood glucose concentration plays a role in the regulation of gastrointestinal motility and sensation. (+info)

Time-dependent and tissue-specific effects of circulating glucose on fetal ovine glucose transporters. (4/3915)

To determine the cellular adaptations to fetal hyperglycemia and hypoglycemia, we examined the time-dependent effects on basal (GLUT-1 and GLUT-3) and insulin-responsive (GLUT-4) glucose transporter proteins by quantitative Western blot analysis in fetal ovine insulin-insensitive (brain and liver) and insulin-sensitive (myocardium, skeletal muscle, and adipose) tissues. Maternal glucose infusions causing fetal hyperglycemia resulted in a transient 30% increase in brain GLUT-1 but not GLUT-3 levels and a decline in liver and adipose GLUT-1 and myocardial and skeletal muscle GLUT-1 and GLUT-4 levels compared with gestational age-matched controls. Maternal insulin infusions leading to fetal hypoglycemia caused a decline in brain GLUT-3, an increase in brain GLUT-1, and a subsequent decline in liver GLUT-1, with no significant change in insulin-sensitive myocardium, skeletal muscle, and adipose tissue GLUT-1 or GLUT-4 concentrations, compared with gestational age-matched sham controls. We conclude that fetal glucose transporters are subject to a time-dependent and tissue- and isoform-specific differential regulation in response to altered circulating glucose and/or insulin concentrations. These cellular adaptations in GLUT-1 (and GLUT-3) are geared toward protecting the conceptus from perturbations in substrate availability, and the adaptations in GLUT-4 are geared toward development of fetal insulin resistance. (+info)

Brain-derived neurotrophic factor improves blood glucose control and alleviates fasting hyperglycemia in C57BLKS-Lepr(db)/lepr(db) mice. (5/3915)

Systemic administration of brain-derived neurotrophic factor (BDNF) decreases nonfasted blood glucose in obese, non-insulin-dependent diabetic C57BLKS-Lepr(db)/lepr(db) (db/db) mice, with a concomitant decrease in body weight. By measuring percent HbA1c in BDNF-treated and pair-fed animals, we show that the effects of BDNF on nonfasted blood glucose levels are not caused by decreased food intake but reflect a significant improvement in blood glucose control. Furthermore, once established, this effect can persist for weeks after cessation of BDNF treatment. Oral glucose tolerance tests were performed to examine the effects of BDNF on blood glucose control in the fasted state and after an oral glucose challenge. BDNF treatment normalized fasting blood glucose from initially hyperglycemic levels and also showed evidence for beneficial, although less marked, effects on the ability to remove exogenous glucose from blood. One means to lower fasting blood glucose is to reduce the glucose output of peripheral tissues that normally play a part in the maintenance of fasting hyperglycemia. Because the liver is the major endogenous source of glucose in blood during fasting, and because hepatic weight and glucose output are increased in type 2 diabetes, we evaluated the effects of BDNF on liver tissue. BDNF reduced the hepatomegaly present in db/db mice, in association with reduced liver glycogen and reduced liver enzyme activity in serum, supporting the possible involvement of liver tissue in the mechanism of action for BDNF. (+info)

Hyperglycemia inhibits insulin activation of Akt/protein kinase B but not phosphatidylinositol 3-kinase in rat skeletal muscle. (6/3915)

Sustained hyperglycemia impairs insulin-stimulated glucose utilization in the skeletal muscle of both humans and experimental animals--a phenomenon referred to clinically as glucose toxicity. To study how this occurs, a model was developed in which hyperglycemia produces insulin resistance in vitro. Rat extensor digitorum longus muscles were preincubated for 4 h in Krebs-Henseleit solution containing glucose or glucose + insulin at various concentrations, after which insulin action was studied. Preincubation with 25 mmol/l glucose + insulin (10 mU/ml) led to a 70% decrease in the ability of insulin (10 mU/ml) to stimulate glucose incorporation into glycogen and a 30% decrease in 2-deoxyglucose (2-DG) uptake, compared with muscles incubated with 0 mmol/l glucose. Glucose incorporation into lipid and its oxidation to CO2 were marginally diminished, if at all. The alterations of glycogen synthesis and 2-DG uptake were first evident after 1 h and were maximal after 2 h of preincubation; they were not observed in muscles preincubated with 25 mmol/l glucose + insulin for 5 min. Preincubation for 4 h with 25 mmol/l glucose in the absence of insulin produced a similar although somewhat smaller decrease in insulin-stimulated glycogen synthesis; however, it did not alter 2-DG uptake, glucose oxidation to CO2, or incorporation into lipids. Studies of insulin signaling in the latter muscles revealed that activation of Akt/protein kinase B (PKB) was diminished by 60%, compared with that of muscles preincubated in a glucose-free medium; whereas activation of phosphatidylinositol (PI) 3-kinase, an upstream regulator of Akt/PKB in the insulin-signaling cascade, and of mitogen-activated protein (MAP) kinase, a parallel signal, was unaffected. Immunoblots demonstrated that this was not due to a change in Akt/PKB abundance. The results indicate that hyperglycemia-induced insulin resistance can be studied in rat skeletal muscle in vitro. They suggest that impairment of insulin action in these muscles is related to inhibition of Akt/PKB by events that do not affect PI 3-kinase. (+info)

Hyperglycemia and focal brain ischemia. (7/3915)

The influence of hyperglycemic ischemia on tissue damage and cerebral blood flow was studied in rats subjected to short-lasting transient middle cerebral artery (MCA) occlusion. Rats were made hyperglycemic by intravenous infusion of glucose to a blood glucose level of about 20 mmol/L, and MCA occlusion was performed with the intraluminar filament technique for 15, 30, or 60 minutes, followed by 7 days of recovery. Normoglycemic animals received saline infusion. Perfusion-fixed brains were examined microscopically, and the volumes of selective neuronal necrosis and infarctions were calculated. Cerebral blood flow was measured autoradiographically at the end of 30 minutes of MCA occlusion and after 1 hour of recirculation in normoglycemic and hyperglycemic animals. In two additional groups with 30 minutes of MCA occlusion, CO2 was added to the inhaled gases to create a similar tissue acidosis as in hyperglycemic animals. In one group CBF was measured, and the second group was examined for tissue damage after 7 days. Fifteen and 30 minutes of MCA occlusion in combination with hyperglycemia produced larger infarcts and smaller amounts of selective neuronal necrosis than in rats with normal blood glucose levels, a significant difference in the total volume of ischemic damage being found after 30 minutes of MCA occlusion. After 60 minutes of occlusion, when the volume of infarction was larger, only minor differences between normoglycemic and hyperglycemic animals were found. Hypercapnic animals showed volumes of both selective neuronal necrosis and infarction that were almost identical with those observed in normoglycemic, normocapnic animals. When local CBF was measured in the ischemic core after 30 minutes of occlusion, neither the hyperglycemic nor the hypercapnic animals were found to be significantly different from the normoglycemic group. Brief focal cerebral ischemia combined with hyperglycemia leads to larger and more severe tissue damage. Our results do not support the hypothesis that the aggravated injury is caused by any disturbances in CBF. (+info)

Renal changes on hyperglycemia and angiotensin-converting enzyme in type 1 diabetes. (8/3915)

Hyperglycemia causes capillary vasodilation and high glomerular capillary hydraulic pressure, which lead to glomerulosclerosis and hypertension in type 1 diabetic subjects. The insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene can modulate risk of nephropathy due to hyperglycemia, and the II genotype (producing low plasma ACE concentrations and probably reduced renal angiotensin II generation and kinin inactivation) may protect against diabetic nephropathy. We tested the possible interaction between ACE I/D polymorphism and uncontrolled type 1 diabetes by measuring glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) during normoglycemia ( approximately 5 mmol/L) and hyperglycemia ( approximately 15 mmol/L) in 9 normoalbuminuric, normotensive type 1 diabetic subjects with the II genotype and 18 matched controls with the ID or DD genotype. Baseline GFR (145+/-22 mL/min per 1.73 m2) and ERPF (636+/-69 mL/min per 1.73 m2) of II subjects declined by 8+/-10% and 10+/-9%, respectively, during hyperglycemia; whereas baseline GFR (138+/-16 mL/min per 1.73 m2) and ERPF (607+/-93 mL/min per 1.73 m2) increased by 4+/-7% and 6+/-11%, respectively, in ID and DD subjects (II versus ID or DD subjects: P=0.0007 and P=0.0005, for GFR and ERPF, respectively). The changes in renal hemodynamics of subjects carrying 1 or 2 D alleles were compatible, with a mainly preglomerular vasodilation induced by hyperglycemia, proportional to plasma ACE concentration (P=0.024); this was not observed in subjects with the II genotype. Thus, type 1 diabetic individuals with the II genotype are resistant to glomerular changes induced by hyperglycemia, providing a basis for their reduced risk of nephropathy. (+info)

There are several possible causes of hyperglycemia, including:

1. Diabetes: This is a chronic condition where the body either does not produce enough insulin or cannot use insulin effectively.
2. Insulin resistance: This occurs when the body's cells become less responsive to insulin, leading to high blood sugar levels.
3. Pancreatitis: This is inflammation of the pancreas, which can lead to high blood sugar levels.
4. Cushing's syndrome: This is a rare hormonal disorder that can cause high blood sugar levels.
5. Medications: Certain medications, such as steroids and some types of antidepressants, can raise blood sugar levels.
6. Stress: Stress can cause the release of hormones such as cortisol and adrenaline, which can raise blood sugar levels.
7. Infections: Certain infections, such as pneumonia or urinary tract infections, can cause high blood sugar levels.
8. Trauma: Traumatic injuries can cause high blood sugar levels due to the release of stress hormones.
9. Surgery: Some types of surgery, such as heart bypass surgery, can cause high blood sugar levels.
10. Pregnancy: High blood sugar levels can occur during pregnancy, especially in women who have a history of gestational diabetes.

Hyperglycemia can cause a range of symptoms, including:

1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Headaches
5. Cuts or bruises that are slow to heal
6. Tingling or numbness in the hands and feet
7. Dry, itchy skin
8. Flu-like symptoms, such as weakness, dizziness, and stomach pain
9. Recurring skin, gum, or bladder infections
10. Sexual dysfunction in men and women

If left untreated, hyperglycemia can lead to serious complications, including:

1. Diabetic ketoacidosis (DKA): A life-threatening condition that occurs when the body produces high levels of ketones, which are acidic substances that can cause confusion, nausea, and vomiting.
2. Hypoglycemia: Low blood sugar levels that can cause dizziness, confusion, and even loss of consciousness.
3. Nerve damage: High blood sugar levels over an extended period can damage the nerves, leading to numbness, tingling, and pain in the hands and feet.
4. Kidney damage: The kidneys may become overworked and damaged if they are unable to filter out the excess glucose in the blood.
5. Eye damage: High blood sugar levels can cause damage to the blood vessels in the eyes, leading to vision loss and blindness.
6. Cardiovascular disease: Hyperglycemia can increase the risk of cardiovascular disease, including heart attacks, strokes, and peripheral artery disease.
7. Cognitive impairment: Hyperglycemia has been linked to cognitive impairment and an increased risk of dementia.

It is essential to manage hyperglycemia by making lifestyle changes, such as following a healthy diet, regular exercise, and taking medication if prescribed by a healthcare professional. Monitoring blood sugar levels regularly can help identify the signs of hyperglycemia and prevent long-term complications.

Types of Experimental Diabetes Mellitus include:

1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.

Experimental Diabetes Mellitus has several applications in research, including:

1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.

In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.

Type 2 diabetes can be managed through a combination of diet, exercise, and medication. In some cases, lifestyle changes may be enough to control blood sugar levels, while in other cases, medication or insulin therapy may be necessary. Regular monitoring of blood sugar levels and follow-up with a healthcare provider are important for managing the condition and preventing complications.

Common symptoms of type 2 diabetes include:

* Increased thirst and urination
* Fatigue
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet
* Recurring skin, gum, or bladder infections

If left untreated, type 2 diabetes can lead to a range of complications, including:

* Heart disease and stroke
* Kidney damage and failure
* Nerve damage and pain
* Eye damage and blindness
* Foot damage and amputation

The exact cause of type 2 diabetes is not known, but it is believed to be linked to a combination of genetic and lifestyle factors, such as:

* Obesity and excess body weight
* Lack of physical activity
* Poor diet and nutrition
* Age and family history
* Certain ethnicities (e.g., African American, Hispanic/Latino, Native American)
* History of gestational diabetes or delivering a baby over 9 lbs.

There is no cure for type 2 diabetes, but it can be managed and controlled through a combination of lifestyle changes and medication. With proper treatment and self-care, people with type 2 diabetes can lead long, healthy lives.

There are several types of diabetes mellitus, including:

1. Type 1 DM: This is an autoimmune condition in which the body's immune system attacks and destroys the cells in the pancreas that produce insulin, resulting in a complete deficiency of insulin production. It typically develops in childhood or adolescence, and patients with this condition require lifelong insulin therapy.
2. Type 2 DM: This is the most common form of diabetes, accounting for around 90% of all cases. It is caused by a combination of insulin resistance (where the body's cells do not respond properly to insulin) and impaired insulin secretion. It is often associated with obesity, physical inactivity, and a diet high in sugar and unhealthy fats.
3. Gestational DM: This type of diabetes develops during pregnancy, usually in the second or third trimester. Hormonal changes and insulin resistance can cause blood sugar levels to rise, putting both the mother and baby at risk.
4. LADA (Latent Autoimmune Diabetes in Adults): This is a form of type 1 DM that develops in adults, typically after the age of 30. It shares features with both type 1 and type 2 DM.
5. MODY (Maturity-Onset Diabetes of the Young): This is a rare form of diabetes caused by genetic mutations that affect insulin production. It typically develops in young adulthood and can be managed with lifestyle changes and/or medication.

The symptoms of diabetes mellitus can vary depending on the severity of the condition, but may include:

1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Cuts or bruises that are slow to heal
5. Tingling or numbness in hands and feet
6. Recurring skin, gum, or bladder infections
7. Flu-like symptoms such as weakness, dizziness, and stomach pain
8. Dark, velvety skin patches (acanthosis nigricans)
9. Yellowish color of the skin and eyes (jaundice)
10. Delayed healing of cuts and wounds

If left untreated, diabetes mellitus can lead to a range of complications, including:

1. Heart disease and stroke
2. Kidney damage and failure
3. Nerve damage (neuropathy)
4. Eye damage (retinopathy)
5. Foot damage (neuropathic ulcers)
6. Cognitive impairment and dementia
7. Increased risk of infections and other diseases, such as pneumonia, gum disease, and urinary tract infections.

It is important to note that not all individuals with diabetes will experience these complications, and that proper management of the condition can greatly reduce the risk of developing these complications.

Symptoms of type 1 diabetes can include increased thirst and urination, blurred vision, fatigue, weight loss, and skin infections. If left untreated, type 1 diabetes can lead to serious complications such as kidney damage, nerve damage, and blindness.

Type 1 diabetes is diagnosed through a combination of physical examination, medical history, and laboratory tests such as blood glucose measurements and autoantibody tests. Treatment typically involves insulin therapy, which can be administered via injections or an insulin pump, as well as regular monitoring of blood glucose levels and appropriate lifestyle modifications such as a healthy diet and regular exercise.

In extreme cases, hypoglycemia can lead to seizures, loss of consciousness, and even coma. It is important to recognize the symptoms of hypoglycemia early on and seek medical attention if they persist or worsen over time. Treatment typically involves raising blood sugar levels through the consumption of quick-acting carbohydrates such as glucose tablets, fruit juice, or hard candy.

If left untreated, hypoglycemia can have serious consequences, including long-term damage to the brain, heart, and other organs. It is important for individuals with diabetes to monitor their blood sugar levels regularly and work with their healthcare provider to manage their condition effectively.

In hyperinsulinism, the body produces too much insulin, leading to a range of symptoms including:

1. Hypoglycemia (low blood sugar): Excessive insulin can cause blood sugar levels to drop too low, leading to hypoglycemic symptoms such as shakiness, dizziness, confusion, and rapid heartbeat.
2. Weight gain: Hyperinsulinism can lead to weight gain due to the body's inability to effectively use glucose for energy production.
3. Fatigue: Excessive insulin can cause fatigue, as the body's cells are not able to effectively use glucose for energy production.
4. Mood changes: Hyperinsulinism can lead to mood changes such as irritability, anxiety, and depression.
5. Polycystic ovary syndrome (PCOS): Women with PCOS are at a higher risk of developing hyperinsulinism due to insulin resistance.
6. Gestational diabetes: Hyperinsulinism can occur during pregnancy, leading to gestational diabetes.
7. Acanthosis nigricans: A condition characterized by dark, velvety patches on the skin, often found in the armpits, neck, and groin area.
8. Cancer: Hyperinsulinism has been linked to an increased risk of certain types of cancer, such as breast, colon, and pancreatic cancer.
9. Cardiovascular disease: Excessive insulin can increase the risk of cardiovascular disease, including high blood pressure, heart disease, and stroke.
10. Cognitive impairment: Hyperinsulinism has been linked to cognitive impairment and an increased risk of dementia.

There are several causes of hyperinsulinism, including:

1. Insulin-producing tumors: Tumors that produce excessive amounts of insulin can lead to hyperinsulinism.
2. Familial hyperinsulinism: A genetic disorder that affects the regulation of insulin secretion and action.
3. Pancreatic beta-cell dysfunction: Dysfunction in the pancreatic beta cells, which produce insulin, can lead to hyperinsulinism.
4. Medications: Certain medications such as steroids and certain psychiatric drugs can cause hyperinsulinism.
5. Pituitary tumors: Tumors in the pituitary gland can lead to excessive secretion of growth hormone, which can stimulate insulin production.
6. Maternal diabetes during pregnancy: Women with diabetes during pregnancy may experience hyperinsulinism due to increased insulin resistance and higher insulin levels.
7. Gestational diabetes: High blood sugar during pregnancy can lead to hyperinsulinism.
8. Polycystic ovary syndrome (PCOS): Women with PCOS may experience hyperinsulinism due to insulin resistance and high insulin levels.
9. Cushing's syndrome: An endocrine disorder caused by excessive cortisol production can lead to hyperinsulinism.
10. Other medical conditions: Certain medical conditions such as thyroid disorders, adrenal gland disorders, and pituitary gland disorders can also cause hyperinsulinism.

It's important to note that some individuals with hyperinsulinism may not experience any symptoms, while others may experience a range of symptoms, including:

1. Weight gain
2. Fatigue
3. Headaches
4. Numbness or tingling in the hands and feet
5. Memory loss and difficulty concentrating
6. Mood changes, such as anxiety and depression
7. Skin problems, such as acne and thinning skin
8. Increased risk of heart disease and stroke
9. Growth retardation in children
10. Increased risk of developing type 2 diabetes

If you suspect that you or your child may have hyperinsulinism, it's important to consult with a healthcare professional for proper diagnosis and treatment. A doctor may perform a physical examination, take a medical history, and order blood tests to determine if hyperinsulinism is present and what may be causing it. Treatment options for hyperinsulinism will depend on the underlying cause of the condition. In some cases, medications such as metformin or other anti-diabetic drugs may be prescribed to help regulate blood sugar levels and reduce insulin production. In other cases, surgery or lifestyle changes may be necessary. With proper diagnosis and treatment, it is possible to manage hyperinsulinism and prevent or manage related health complications.

There are several factors that can contribute to the development of insulin resistance, including:

1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.

There are several ways to diagnose insulin resistance, including:

1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.

There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:

1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.

Medications that may be used to treat insulin resistance include:

1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.

It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.

1. Heart Disease: High blood sugar levels can damage the blood vessels and increase the risk of heart disease, which includes conditions like heart attacks, strokes, and peripheral artery disease.
2. Kidney Damage: Uncontrolled diabetes can damage the kidneys over time, leading to chronic kidney disease and potentially even kidney failure.
3. Nerve Damage: High blood sugar levels can damage the nerves in the body, causing numbness, tingling, and pain in the hands and feet. This is known as diabetic neuropathy.
4. Eye Problems: Diabetes can cause changes in the blood vessels of the eyes, leading to vision problems and even blindness. This is known as diabetic retinopathy.
5. Infections: People with diabetes are more prone to developing skin infections, urinary tract infections, and other types of infections due to their weakened immune system.
6. Amputations: Poor blood flow and nerve damage can lead to amputations of the feet or legs if left untreated.
7. Cognitive Decline: Diabetes has been linked to an increased risk of cognitive decline and dementia.
8. Sexual Dysfunction: Men with diabetes may experience erectile dysfunction, while women with diabetes may experience decreased sexual desire and vaginal dryness.
9. Gum Disease: People with diabetes are more prone to developing gum disease and other oral health problems due to their increased risk of infection.
10. Flu and Pneumonia: Diabetes can weaken the immune system, making it easier to catch the flu and pneumonia.

It is important for people with diabetes to manage their condition properly to prevent or delay these complications from occurring. This includes monitoring blood sugar levels regularly, taking medication as prescribed by a doctor, and following a healthy diet and exercise plan. Regular check-ups with a healthcare provider can also help identify any potential complications early on and prevent them from becoming more serious.

There are several types of diabetic angiopathies, including:

1. Peripheral artery disease (PAD): This occurs when the blood vessels in the legs and arms become narrowed or blocked, leading to reduced blood flow and oxygen supply to the limbs.
2. Peripheral neuropathy: This is damage to the nerves in the hands and feet, which can cause pain, numbness, and weakness.
3. Retinopathy: This is damage to the blood vessels in the retina, which can lead to vision loss and blindness.
4. Nephropathy: This is damage to the kidneys, which can lead to kidney failure and the need for dialysis.
5. Cardiovascular disease: This includes heart attack, stroke, and other conditions that affect the heart and blood vessels.

The risk of developing diabetic angiopathies increases with the duration of diabetes and the level of blood sugar control. Other factors that can increase the risk include high blood pressure, high cholesterol, smoking, and a family history of diabetes-related complications.

Symptoms of diabetic angiopathies can vary depending on the specific type of complication and the location of the affected blood vessels or nerves. Common symptoms include:

* Pain or discomfort in the arms, legs, hands, or feet
* Numbness or tingling sensations in the hands and feet
* Weakness or fatigue in the limbs
* Difficulty healing wounds or cuts
* Vision changes or blindness
* Kidney problems or failure
* Heart attack or stroke

Diagnosis of diabetic angiopathies typically involves a combination of physical examination, medical history, and diagnostic tests such as ultrasound, MRI, or CT scans. Treatment options vary depending on the specific type of complication and may include:

* Medications to control blood sugar levels, high blood pressure, and high cholesterol
* Lifestyle changes such as a healthy diet and regular exercise
* Surgery to repair or bypass affected blood vessels or nerves
* Dialysis for kidney failure
* In some cases, amputation of the affected limb

Preventing diabetic angiopathies involves managing diabetes effectively through a combination of medication, lifestyle changes, and regular medical check-ups. Early detection and treatment can help prevent or delay the progression of complications.

1. Impaired glucose tolerance (IGT): This is a condition where the body has difficulty regulating blood sugar levels after consuming a meal.
2. Impaired fasting glucose (IFG): This is a condition where the body has difficulty regulating blood sugar levels when fasting (not eating for a period of time).
3. Gestational diabetes: This is a type of diabetes that develops during pregnancy, usually in the second or third trimester.
4. Type 2 diabetes: This is a chronic condition where the body cannot effectively use insulin to regulate blood sugar levels.

The symptoms of glucose intolerance can vary depending on the type and severity of the condition. Some common symptoms include:

* High blood sugar levels
* Increased thirst and urination
* Fatigue
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet

The diagnosis of glucose intolerance is typically made through a combination of physical examination, medical history, and laboratory tests such as:

* Fasting plasma glucose (FPG) test: This measures the level of glucose in the blood after an overnight fast.
* Oral glucose tolerance test (OGTT): This measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
* Hemoglobin A1c (HbA1c) test: This measures the average blood sugar level over the past 2-3 months.

Treatment for glucose intolerance usually involves lifestyle changes such as:

* Eating a healthy, balanced diet that is low in added sugars and refined carbohydrates
* Increasing physical activity to help the body use insulin more effectively
* Losing weight if you are overweight or obese
* Monitoring blood sugar levels regularly

In some cases, medication may be prescribed to help manage blood sugar levels. These include:

* Metformin: This is a type of oral medication that helps the body use insulin more effectively.
* Sulfonylureas: These medications stimulate the release of insulin from the pancreas.
* Thiazolidinediones: These medications improve the body's sensitivity to insulin.

If left untreated, glucose intolerance can lead to a range of complications such as:

* Type 2 diabetes: This is a more severe form of glucose intolerance that can cause damage to the body's organs and tissues.
* Cardiovascular disease: High blood sugar levels can increase the risk of heart disease and stroke.
* Nerve damage: High blood sugar levels over an extended period can damage the nerves, leading to numbness, tingling, and pain in the hands and feet.
* Kidney damage: High blood sugar levels can damage the kidneys and lead to kidney disease.
* Eye damage: High blood sugar levels can damage the blood vessels in the eyes, leading to vision problems.

It is important to note that not everyone with glucose intolerance will develop these complications, but it is important to manage the condition to reduce the risk of these complications occurring.

HHNK coma can occur in people with type 1 or type 2 diabetes who have poorly controlled blood sugar levels over an extended period. It is more common in people who are not taking insulin or other diabetic medications as prescribed, or those who have a history of diabetic ketoacidosis (DKA).

The symptoms of HHNK coma can vary depending on the severity of the condition, but they may include:

* Confusion, disorientation, or decreased consciousness
* Slurred speech or difficulty speaking
* Seizures or convulsions
* Vision changes or blindness
* Headache, nausea, and vomiting
* Dry mouth and skin
* High blood pressure (hypertension)
* Rapid heart rate (tachycardia)
* Low body temperature (hypothermia)

If left untreated, HHNK coma can lead to severe complications such as cerebral edema, seizures, and even death. Treatment typically involves hospitalization and aggressive management of blood sugar levels, fluids, and electrolytes. In some cases, insulin therapy may be necessary to bring blood sugar levels back to normal.

The diagnosis of HHNK coma is based on a combination of clinical findings, laboratory tests, and medical imaging studies. Laboratory tests may include measurements of blood sugar levels, electrolytes, and osmolality. Medical imaging studies such as CT or MRI scans may be used to assess the brain for signs of injury or swelling.

The prevention of HHNK coma is crucial in managing the condition. This includes close monitoring of blood sugar levels, proper management of diabetes, and prompt treatment of any underlying medical conditions that may predispose a patient to developing HHNK coma. In addition, patients with known risk factors such as hypoglycemia or diabetic ketoacidosis should be educated about the signs and symptoms of HHNK coma and be instructed on how to seek medical attention promptly if they experience any symptoms.

Overall, HHNK coma is a serious medical condition that requires prompt recognition and treatment to prevent complications and improve outcomes. It is important for healthcare professionals to be aware of the signs and symptoms of HHNK coma and to provide appropriate management and education to patients at risk.

There are several types of diabetic nephropathy, including:

1. Mesangial proliferative glomerulonephritis: This is the most common type of diabetic nephropathy and is characterized by an overgrowth of cells in the mesangium, a part of the glomerulus (the blood-filtering unit of the kidney).
2. Segmental sclerosis: This type of diabetic nephropathy involves the hardening of some parts of the glomeruli, leading to decreased kidney function.
3. Fibrotic glomerulopathy: This is a rare form of diabetic nephropathy that is characterized by the accumulation of fibrotic tissue in the glomeruli.
4. Membranous nephropathy: This type of diabetic nephropathy involves the deposition of immune complexes (antigen-antibody complexes) in the glomeruli, leading to inflammation and damage to the kidneys.
5. Minimal change disease: This is a rare form of diabetic nephropathy that is characterized by minimal changes in the glomeruli, but with significant loss of kidney function.

The symptoms of diabetic nephropathy can be non-specific and may include proteinuria (excess protein in the urine), hematuria (blood in the urine), and decreased kidney function. Diagnosis is typically made through a combination of physical examination, medical history, laboratory tests, and imaging studies such as ultrasound or CT scans.

Treatment for diabetic nephropathy typically involves managing blood sugar levels through lifestyle changes (such as diet and exercise) and medication, as well as controlling high blood pressure and other underlying conditions. In severe cases, dialysis or kidney transplantation may be necessary. Early detection and management of diabetic nephropathy can help slow the progression of the disease and improve outcomes for patients with this condition.

Symptoms of DKA can include:

* High blood sugar levels (usually above 300 mg/dL)
* High levels of ketones in the blood and urine
* Nausea, vomiting, and abdominal pain
* Fatigue, weakness, and confusion
* Headache and dry mouth
* Flu-like symptoms, such as fever, chills, and muscle aches

If left untreated, DKA can lead to serious complications, such as:

* Dehydration and electrolyte imbalances
* Seizures and coma
* Kidney damage and failure

Treatment of DKA typically involves hospitalization and intravenous fluids to correct dehydration and electrolyte imbalances. Insulin therapy is also started to lower blood sugar levels and promote the breakdown of ketones. In severe cases, medications such as sodium bicarbonate may be given to help neutralize the excess ketones in the blood.

Preventing DKA involves proper management of diabetes, including:

* Taking insulin as prescribed and monitoring blood sugar levels regularly
* Maintaining a healthy diet and exercise program
* Monitoring for signs of infection or illness, which can increase the risk of DKA

Early detection and treatment of DKA are critical to preventing serious complications and improving outcomes for people with diabetes.

Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.

There are several ways to measure body weight, including:

1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.

It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.

Pregnancy in diabetics is typically classified into three categories:

1. Gestational diabetes mellitus (GDM): This type of diabetes develops during pregnancy, typically after 24 weeks of gestation. It is caused by hormonal changes that interfere with insulin's ability to regulate blood sugar levels.
2. Pre-existing diabetes: Women who have already been diagnosed with diabetes before becoming pregnant are considered to have pre-existing diabetes. This type of diabetes can be either type 1 or type 2.
3. Type 1 diabetes in pregnancy: Type 1 diabetes is an autoimmune condition that typically develops in childhood or young adulthood. Women who have type 1 diabetes and become pregnant require careful management of their blood sugar levels to ensure the health of both themselves and their baby.

Pregnancy in diabetics requires close monitoring and careful management throughout the pregnancy. Regular check-ups with a healthcare provider are essential to identify any potential complications early on and prevent them from becoming more serious. Some of the common complications associated with pregnancy in diabetics include:

1. Gestational hypertension: This is a type of high blood pressure that develops during pregnancy, particularly in women who have gestational diabetes. It can increase the risk of preeclampsia and other complications.
2. Preeclampsia: This is a serious condition that can cause damage to organs such as the liver, kidneys, and brain. Women with pre-existing diabetes are at higher risk of developing preeclampsia.
3. Macrosomia: As mentioned earlier, this is a condition where the baby grows larger than average, which can increase the risk of complications during delivery.
4. Hypoglycemia: This is a condition where the blood sugar levels become too low, which can be dangerous for both the mother and the baby.
5. Jaundice: This is a condition that causes yellowing of the skin and eyes due to high bilirubin levels in the blood. It is more common in newborns of diabetic mothers.
6. Respiratory distress syndrome: This is a condition where the baby's lungs are not fully developed, which can lead to breathing difficulties.
7. Type 2 diabetes: Women who develop gestational diabetes during pregnancy are at higher risk of developing type 2 diabetes later in life.
8. Cholestasis of pregnancy: This is a condition where the liver produces too much bile, which can cause itching and liver damage. It is more common in women with gestational diabetes.
9. Premature birth: Babies born to mothers with diabetes are at higher risk of being born prematurely, which can increase the risk of complications.
10. Congenital anomalies: There is an increased risk of certain birth defects in babies born to mothers with diabetes, such as heart and brain defects.

It's important for pregnant women who have been diagnosed with gestational diabetes to work closely with their healthcare provider to manage their condition and reduce the risks associated with it. This may involve monitoring blood sugar levels regularly, taking insulin or other medications as prescribed, and making any necessary lifestyle changes.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

There are several different types of obesity, including:

1. Central obesity: This type of obesity is characterized by excess fat around the waistline, which can increase the risk of health problems such as type 2 diabetes and cardiovascular disease.
2. Peripheral obesity: This type of obesity is characterized by excess fat in the hips, thighs, and arms.
3. Visceral obesity: This type of obesity is characterized by excess fat around the internal organs in the abdominal cavity.
4. Mixed obesity: This type of obesity is characterized by both central and peripheral obesity.

Obesity can be caused by a variety of factors, including genetics, lack of physical activity, poor diet, sleep deprivation, and certain medications. Treatment for obesity typically involves a combination of lifestyle changes, such as increased physical activity and a healthy diet, and in some cases, medication or surgery may be necessary to achieve weight loss.

Preventing obesity is important for overall health and well-being, and can be achieved through a variety of strategies, including:

1. Eating a healthy, balanced diet that is low in added sugars, saturated fats, and refined carbohydrates.
2. Engaging in regular physical activity, such as walking, jogging, or swimming.
3. Getting enough sleep each night.
4. Managing stress levels through relaxation techniques, such as meditation or deep breathing.
5. Avoiding excessive alcohol consumption and quitting smoking.
6. Monitoring weight and body mass index (BMI) on a regular basis to identify any changes or potential health risks.
7. Seeking professional help from a healthcare provider or registered dietitian for personalized guidance on weight management and healthy lifestyle choices.

Chorea is a type of movement disorder that is characterized by brief, jerky movements of the limbs or other parts of the body. It is often associated with neurological conditions such as Huntington's disease, but can also be caused by other factors such as medication side effects or metabolic disorders.

The term "chorea" comes from the Greek word for "dance," and refers to the irregular, involuntary nature of these movements. People with chorea may experience a wide range of symptoms, including twitching, jerking, writhing, or other types of uncontrolled movements. In some cases, these movements can be so severe that they interfere with daily activities and quality of life.

There are several different types of chorea, including:

1. Huntington's disease chorea: This is the most common type of chorea, and is associated with a genetic disorder called Huntington's disease.
2. Sydenham's chorea: This type of chorea is associated with rheumatic fever, a bacterial infection that can damage the heart and other organs.
3. Chorea gravidarum: This type of chorea occurs during pregnancy and is thought to be caused by changes in hormone levels.
4. Chorea-acanthocytosis: This is a rare genetic disorder that causes chorea, as well as other symptoms such as acanthocytes (abnormal red blood cells).
5. Chorea-ballism: This is a rare movement disorder that is characterized by brief, jerky movements of the limbs, as well as slow, writhing movements of the trunk and head.

There are several different ways to diagnose chorea, including:

1. Physical examination: A doctor may observe the patient's movements and ask them to perform specific tasks in order to assess their symptoms.
2. Imaging tests: Such as MRI or CT scans, to rule out other conditions that may cause similar symptoms.
3. Genetic testing: To identify genetic causes of chorea, such as Huntington's disease or other inherited disorders.
4. Blood tests: To check for infections or other medical conditions that may be contributing to the chorea.
5. Electromyography (EMG): This test measures the electrical activity of muscles and can help determine if there is any damage to the nerves or muscles that are causing the chorea.

Treatment for chorea depends on the underlying cause of the condition, and may include:

1. Antibiotics: To treat bacterial infections that may be contributing to the chorea.
2. Antipsychotic medications: These drugs can help reduce the severity of symptoms in some cases of chorea.
3. Anticholinergic medications: These drugs can help reduce muscle stiffness and tremors, which are common symptoms of chorea.
4. Physical therapy: This may be helpful in improving movement and coordination.
5. Surgery: In some cases, surgery may be necessary to treat the underlying cause of the chorea, such as a tumor or cerebral palsy.

In summary, chorea is a movement disorder that can be caused by a variety of factors, and treatment depends on the underlying cause of the condition. It is important to seek medical attention if you or someone you know is experiencing involuntary movements or other symptoms of chorea, as early diagnosis and treatment can improve outcomes.

The American Diabetes Association (ADA) defines prediabetes as having a fasting blood sugar level of 100-125 mg/dL or a 2-hour postprandial (after meal) blood sugar level of 140-199 mg/dL.

The prediabetic state is characterized by insulin resistance, which means that the body's cells are not able to effectively use insulin, a hormone produced by the pancreas that regulates blood sugar levels. As a result, blood sugar levels begin to rise, but not high enough to be classified as diabetes.

Prediabetes is a reversible condition, and individuals with this condition can take steps to lower their blood sugar levels and prevent the development of type 2 diabetes. Lifestyle changes such as losing weight, increasing physical activity, and following a healthy diet can help improve insulin sensitivity and reduce the risk of developing diabetes. In some cases, medication may also be prescribed to help lower blood sugar levels.

It's important to note that not everyone with prediabetes will develop type 2 diabetes, but it is a significant risk factor. Early detection and intervention can help prevent or delay the progression to type 2 diabetes, and improve overall health outcomes.

There are two main types of DR:

1. Non-proliferative diabetic retinopathy (NPDR): This is the early stage of DR, where the blood vessels in the retina become damaged and start to leak fluid or bleed. The symptoms can be mild or severe and may include blurred vision, floaters, and flashes of light.
2. Proliferative diabetic retinopathy (PDR): This is the advanced stage of DR, where new blood vessels start to grow in the retina. These vessels are weak and can cause severe bleeding, leading to vision loss.

DR is a common complication of diabetes, and it is estimated that up to 80% of people with diabetes will develop some form of DR over their lifetime. The risk of developing DR increases with the duration of diabetes and the level of blood sugar control.

Early detection and treatment of DR can help to prevent vision loss, so it is important for people with diabetes to have regular eye exams to monitor their retinal health. Treatment options for DR include laser surgery, injections of anti-vascular endothelial growth factor (VEGF) medications, and vitrectomy, a surgical procedure to remove the vitreous gel and blood from the eye.

Preventing Diabetic Retinopathy

While there is no surefire way to prevent diabetic retinopathy (DR), there are several steps that people with diabetes can take to reduce their risk of developing this complication:

1. Control blood sugar levels: Keeping blood sugar levels within a healthy range can help to slow the progression of DR. This can be achieved through a combination of diet, exercise, and medication.
2. Monitor blood pressure: High blood pressure can damage the blood vessels in the retina, so it is important to monitor and control blood pressure to reduce the risk of DR.
3. Maintain healthy blood lipids: Elevated levels of low-density lipoprotein (LDL) cholesterol and lower levels of high-density lipoprotein (HDL) cholesterol can increase the risk of DR.
4. Quit smoking: Smoking can damage the blood vessels in the retina and increase the risk of DR.
5. Maintain a healthy weight: Obesity is a risk factor for DR, so maintaining a healthy weight can help to reduce the risk of this complication.
6. Get regular eye exams: Regular eye exams can help to detect DR in its early stages, when it is easier to treat and prevent vision loss.

Preventing Diabetic Retinopathy

While there is no cure for diabetic retinopathy (DR), there are several treatment options available to help manage the condition and prevent vision loss. These include:

1. Laser surgery: This is a common treatment for early-stage DR, where a laser is used to shrink abnormal blood vessels in the retina and reduce the risk of further damage.
2. Injection therapy: Medications such as anti-vascular endothelial growth factor (VEGF) injections can be used to shrink abnormal blood vessels and reduce swelling in the retina.
3. Vitrectomy: In severe cases of DR, a vitrectomy may be performed to remove scar tissue and blood from the center of the eye.
4. Blood pressure control: Maintaining healthy blood pressure can help to slow the progression of DR.
5. Blood glucose control: Keeping blood sugar levels under control can also slow the progression of DR.
6. Follow-up care: Regular follow-up appointments with an eye doctor are important to monitor the progress of DR and adjust treatment as needed.

Early detection and treatment of diabetic retinopathy can help to prevent vision loss and improve outcomes for individuals with this complication of diabetes. By managing blood sugar levels, blood pressure, and cholesterol, and by getting regular eye exams, individuals with diabetes can reduce their risk of developing DR and other diabetic complications.

There are several types of diabetic neuropathies, including:

1. Peripheral neuropathy: This is the most common type of diabetic neuropathy and affects the nerves in the hands and feet. It can cause numbness, tingling, and pain in these areas.
2. Autonomic neuropathy: This type of neuropathy affects the nerves that control involuntary functions, such as digestion, bladder function, and blood pressure. It can cause a range of symptoms, including constipation, diarrhea, urinary incontinence, and sexual dysfunction.
3. Proximal neuropathy: This type of neuropathy affects the nerves in the legs and hips. It can cause weakness, pain, and stiffness in these areas.
4. Focal neuropathy: This type of neuropathy affects a single nerve, often causing sudden and severe pain.

The exact cause of diabetic neuropathies is not fully understood, but it is thought to be related to high blood sugar levels over time. Other risk factors include poor blood sugar control, obesity, smoking, and alcohol consumption. There is no cure for diabetic neuropathy, but there are several treatments available to manage the symptoms and prevent further nerve damage. These treatments may include medications, physical therapy, and lifestyle changes such as regular exercise and a healthy diet.

Some common examples of critical illnesses include:

1. Sepsis: a systemic inflammatory response to an infection that can lead to organ failure and death.
2. Cardiogenic shock: a condition where the heart is unable to pump enough blood to meet the body's needs, leading to serious complications such as heart failure and death.
3. Acute respiratory distress syndrome (ARDS): a condition where the lungs are severely inflamed and unable to provide sufficient oxygen to the body.
4. Multi-system organ failure: a condition where multiple organs in the body fail simultaneously, leading to serious complications and death.
5. Trauma: severe physical injuries sustained in an accident or other traumatic event.
6. Stroke: a sudden interruption of blood flow to the brain that can lead to permanent brain damage and death.
7. Myocardial infarction (heart attack): a blockage of coronary arteries that supply blood to the heart, leading to damage or death of heart muscle cells.
8. Pulmonary embolism: a blockage of the pulmonary artery, which can lead to respiratory failure and death.
9. Pancreatitis: inflammation of the pancreas that can lead to severe abdominal pain, bleeding, and organ failure.
10. Hypovolemic shock: a condition where there is a severe loss of blood or fluid from the body, leading to hypotension, organ failure, and death.

The diagnosis and treatment of critical illnesses require specialized knowledge and skills, and are typically handled by intensive care unit (ICU) teams consisting of critical care physicians, nurses, and other healthcare professionals. The goal of critical care is to provide life-sustaining interventions and support to patients who are critically ill until they recover or until their condition stabilizes.

Examples of acute diseases include:

1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.

Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.

There are several types of hyperlipidemia, including:

1. High cholesterol: This is the most common type of hyperlipidemia and is characterized by elevated levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol.
2. High triglycerides: This type of hyperlipidemia is characterized by elevated levels of triglycerides in the blood. Triglycerides are a type of fat found in the blood that is used for energy.
3. Low high-density lipoprotein (HDL) cholesterol: HDL cholesterol is known as "good" cholesterol because it helps remove excess cholesterol from the bloodstream and transport it to the liver for excretion. Low levels of HDL cholesterol can contribute to hyperlipidemia.

Symptoms of hyperlipidemia may include xanthomas (fatty deposits on the skin), corneal arcus (a cloudy ring around the iris of the eye), and tendon xanthomas (tender lumps under the skin). However, many people with hyperlipidemia have no symptoms at all.

Hyperlipidemia can be diagnosed through a series of blood tests that measure the levels of different types of cholesterol and triglycerides in the blood. Treatment for hyperlipidemia typically involves dietary changes, such as reducing intake of saturated fats and cholesterol, and increasing physical activity. Medications such as statins, fibric acid derivatives, and bile acid sequestrants may also be prescribed to lower cholesterol levels.

In severe cases of hyperlipidemia, atherosclerosis (hardening of the arteries) can occur, which can lead to cardiovascular disease, including heart attacks and strokes. Therefore, it is important to diagnose and treat hyperlipidemia early on to prevent these complications.

Definition:

* A form of diabetes that develops during pregnancy
* Caused by hormonal changes and insulin resistance
* Can lead to complications for both the mother and the baby
* Typically goes away after childbirth

There are two main types of diabetic coma:

1. DKA: This type of coma is more common in people with type 1 diabetes, but it can also occur in people with type 2 diabetes. It is caused by a lack of insulin in the body, which leads to high levels of glucose and ketones in the blood.
2. Hypoglycemic coma: This type of coma is caused by low blood sugar levels, which can occur when people with diabetes take too much insulin or not enough food.

The symptoms of diabetic coma can vary depending on the type, but they may include:

* Confusion and disorientation
* Slurred speech
* Seizures or convulsions
* Difficulty breathing
* High blood sugar levels (DKA) or low blood sugar levels (hypoglycemic coma)

If left untreated, diabetic coma can be fatal. Treatment typically involves addressing the underlying cause of the coma and providing supportive care, such as intravenous fluids and oxygen. In severe cases, hospitalization may be necessary to monitor and treat the condition.

Preventing diabetic coma requires careful management of diabetes, including monitoring blood sugar levels regularly, taking medication as prescribed, and making any necessary lifestyle changes. It is also important to seek medical attention immediately if symptoms of diabetic coma are present.

1. Abdominal obesity (excess fat around the waistline)
2. High blood pressure (hypertension)
3. Elevated fasting glucose (high blood sugar)
4. High serum triglycerides (elevated levels of triglycerides in the blood)
5. Low HDL cholesterol (low levels of "good" cholesterol)

Having three or more of these conditions is considered a diagnosis of metabolic syndrome X. It is estimated that approximately 34% of adults in the United States have this syndrome, and it is more common in women than men. Risk factors for developing metabolic syndrome include obesity, lack of physical activity, poor diet, and a family history of type 2 diabetes or CVD.

The term "metabolic syndrome" was first introduced in the medical literature in the late 1980s, and since then, it has been the subject of extensive research. The exact causes of metabolic syndrome are not yet fully understood, but it is believed to be related to insulin resistance, inflammation, and changes in body fat distribution.

Treatment for metabolic syndrome typically involves lifestyle modifications such as weight loss, regular physical activity, and a healthy diet. Medications such as blood pressure-lowering drugs, cholesterol-lowering drugs, and anti-diabetic medications may also be prescribed if necessary. It is important to note that not everyone with metabolic syndrome will develop type 2 diabetes or CVD, but the risk is increased. Therefore, early detection and treatment are crucial in preventing these complications.

Anatomy7

Organisms5

Diseases30

Chemicals and Drugs31

Analytical, Diagnostic and Therapeutic Techniques and Equipment12

Psychiatry and Psychology1

Phenomena and Processes11

Health Care1

Accelerated intimal hyperplasia and increased endogenous inhibitors for NO synthesis in rabbits with alloxan-induced hyperglycaemia. (1/3915)

Effect of hyperglycemia-hyperinsulinemia on whole body and regional fatty acid metabolism. (2/3915)

Effects of duodenal distension on antropyloroduodenal pressures and perception are modified by hyperglycemia. (3/3915)

Time-dependent and tissue-specific effects of circulating glucose on fetal ovine glucose transporters. (4/3915)

Brain-derived neurotrophic factor improves blood glucose control and alleviates fasting hyperglycemia in C57BLKS-Lepr(db)/lepr(db) mice. (5/3915)

Hyperglycemia inhibits insulin activation of Akt/protein kinase B but not phosphatidylinositol 3-kinase in rat skeletal muscle. (6/3915)

Hyperglycemia and focal brain ischemia. (7/3915)

Renal changes on hyperglycemia and angiotensin-converting enzyme in type 1 diabetes. (8/3915)

No images available that match "hyperglycemia"

Hyperglycemia

Blood Glucose

Diabetes Mellitus, Experimental

Insulin

Glucose

Diabetes Mellitus, Type 2

Hypoglycemic Agents

Streptozocin

Glucose Tolerance Test

Diabetes Mellitus

Diabetes Mellitus, Type 1

Hypoglycemia

Islets of Langerhans

Hyperinsulinism

Glucagon

Insulin Resistance

Insulin-Secreting Cells

Hemoglobin A, Glycosylated

Postprandial Period

Fasting

Diabetes Complications

Glucose Clamp Technique

Diabetic Angiopathies

Glycosuria

Phlorhizin

Gluconeogenesis

Glucokinase

C-Peptide

Glucose Intolerance

Hyperglycemic Hyperosmolar Nonketotic Coma

Diabetic Nephropathies

Diabetic Ketoacidosis

Body Weight

Liver

Alloxan

Rats, Zucker

Rats, Sprague-Dawley

Pregnancy in Diabetics

Time Factors

Disease Models, Animal

Rats, Wistar

Oxidative Stress

Obesity

Pancreas

Hyperglycinemia, Nonketotic

Glucagon-Like Peptide 1

Chorea

Mice, Inbred C57BL

Glycosylation End Products, Advanced

Prediabetic State

Diabetic Retinopathy

Fatty Acids, Nonesterified

Diabetic Neuropathies

Critical Illness

Islets of Langerhans Transplantation

Risk Factors

Fructosamine

Acute Disease

Mice, Obese

Reference Values

Glucose Transporter Type 2

Acarbose

Glycogenolysis

Cells, Cultured

Hyperlipidemias

Infusions, Intravenous

Endothelium, Vascular

Hexosamines

Glycogen

Diabetes, Gestational

Glucose-6-Phosphatase

Dose-Response Relationship, Drug

Liver Glycogen

Homeostasis

Deoxyglucose

Aldehyde Reductase

Metformin

Diabetic Coma

Proinsulin

Sodium-Glucose Transporter 2