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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes mellitus is a complex metabolic syndrome characterised by varying degrees of insulin deficiency, either absolute or relative, and impaired insulin action on protein, lipid and carbohydrate metabolism. Although hyperglycemia is always present during the course of the disease, at least in the early phase it must not be a unique criterion for diagnosis. A normoglycemic patient with hyperinsulinemia associated with obesity or dyslipidemia could be considered as a case of "normoglycemic diabetes" which will develop in time toward hyperglycemia.
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PMID:Proposal for a new classification of diabetes mellitus. 1066 Sep 78

We examined the effects of the potassium channel opener KRN4884 (5-amino-N-[2-(2-chlorophenyl)ethyl]-N'-cyano-3-pyridinecarboxamidine ) on cardiovascular metabolic syndrome (i.e., syndrome X), in rats. High-fructose diet rats developed hypertension, hypertriglyceridemia, increased total cholesterol/HDL (high-density lipoprotein)-cholesterol ratio, and hyperinsulinemia, KRN4884 (0.3-3.0 mg/kg, twice a day for 14 days, p.o.) alleviated the risk factors in fructose-fed rats. Furthermore, fructose-fed rats exhibited impairment of glucose tolerance and excess insulin secretion when loaded with glucose orally. Treatment with KRN4884 (1.0 mg/kg, twice a day for 14 days, p.o.) improved the glucose intolerance and inhibited hypersecretion of insulin in the glucose-loaded, fructose-fed rats. In contrast, KRN4884 (0.3-1.0 mg/kg, twice a day for 10 days, p.o.) did not affect serum triglyceride, cholesterol, glucose, or insulin concentrations in normal rats. LPL (lipoprotein lipase) activities in skeletal muscle and adipose tissue, and HTGL (hepatic triglyceride lipase) activity in liver were measured after administration of KRN4884 or vehicle twice a day for 14 days in fructose-fed rats. KRN4884 caused a significant increase in LPL activity in muscle and tended to increase LPL activity in adipose tissue in fructose-fed rats. HTGL was decreased in fructose-fed rats as compared with normal controls and was unaffected by KRN4884. These findings suggested that KRN4884 enhances insulin sensitivity and LPL activity, which are related to glucose and lipid metabolism and may be useful for the treatment of syndrome X.
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PMID:Effects of the K+ channel opener KRN4884 on the cardiovascular metabolic syndrome model in rats. 1067 63

Some 44% of all patients with elevated blood pressure are overweight. In obesity-related hypertension, sympathicotonia is regularly found, together with elevated intracellular calcium, sodium retention, increased cardiac output (per minute) and a sensitivity to salt. The role played by hyperinsulinemia has apparently been overstated. A primary rise in the minimal vascular resistance suffices to reduce the perfusion of the skeletal musculature and, solely on this basis, to induce insulin resistance. For the treatment of obesity-related hypertension, non-medicinal approaches to weight reduction predominate. Reducing the daily salt intake to 5 g can also bring about a measurable reduction in blood pressure. For the treatment with antihypertensive drugs, beta blockers and diuretics are the initial choice; in the case of pronounced metabolic syndrome, ACE-inhibitors and alpha-1 receptors.
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PMID:[Fat control--an effective antihypertensive strategy. Special recommendations for therapy of the overweight patient]. 1079 42

Metabolic syndrome X is a multifaceted syndrome, which occurs frequently in the general population. It is more common in men than in women. A large segment of the adult population of industrialized countries develops the metabolic syndrome, produced by genetic, hormonal and lifestyle factors such as obesity, physical inactivity and certain nutrient excesses. This disease is characterized by the clustering of insulin resistance and hyperinsulinemia, and is often associated with dyslipidemia (atherogenic plasma lipid profile), essential hypertension, abdominal (visceral) obesity, glucose intolerance or noninsulin-dependent diabetes mellitus and an increased risk of cardiovascular events. Abnormalities of blood coagulation (higher plasminogen activator inhibitor type 1 and fibrinogen levels), hyperuricemia and microalbuminuria have also been found in metabolic syndrome X. This review summarizes the present knowledge of abnormalities in this syndrome. Each risk factor is reviewed, and potential criteria for diagnosis and therapeutic targets are discussed. Because patients with metabolic syndrome X accumulate cardiac risk factors, they should be given special attention in terms of diagnosis and treatment.
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PMID:Metabolic syndrome X: a review. 1086 69

Capillary endothelial cells are thought to limit the transport of insulin across the endothelium, resulting in attenuated insulin action at target sites. Whether endothelial insulin transport is altered in dysglycemic insulin-resistant states is not clear and was therefore investigated in the JCR:LA-cp corpulent male rat, which exhibits the metabolic syndrome of obesity, insulin resistance, hyperlipidemia, and hyperinsulinemia. Lean littermates that did not develop these alterations served as controls. Animals of both groups were normotensive (mean arterial pressure 136+/-2 mmHg). Hearts from obese and lean rats aged 7 (n = 6) or 18 (n = 8) weeks were perfused in vitro at 10 ml/min per gram wet wt over 51 min with Krebs-Henseleit buffer containing 0.1 or 0.5 U human insulin/l (equivalent to 0.6 and 3 nmol/l). Interstitial fluid was collected using a validated method, and interstitial insulin was determined with a radioimmunoassay. At 0.1 U/l, insulin transfer velocity was similar in both experimental groups (half-times of transfer: 11+/-0.2 min in obese and 18+/-4 min in lean rats; NS), but at 0.5 U/l, the respective half-times were 7+/-1 min in lean and 13+/-2 min in obese rats (P < 0.05). The steady-state level of insulin in the interstitium was 34+/-1% of the vascular level at 0.1 U/l and reached the vascular level (102+/-2%) at 0.5 U/l in both lean and obese rats. In rats aged 18 weeks, the half-times of insulin transfer were 31+/-2 and 14+/-l min in obese rats and 10+/-0.3 and 7+/-0.3 min in lean rats (P < 0.05). Again, interstitial steady-state levels were similar in both groups. Finally, postprandial insulin dynamics were simulated over a period of 120 min with a peak concentration of 0.8 U/l in rats aged 27 weeks (n = 4). The maximal interstitial level was 0.38+/-0.02 U/l in lean rats and 0.24+/-0.02 U/l in obese rats (P < 0.05), and a similar difference was noted throughout insulin infusion (areas under the transudate concentration-time curves: 17 and 11 U/min per 1, respectively). These data show, for the first time in a genetic animal model of insulin resistance, that transfer of insulin across the endothelium is substantially delayed in obese insulin-resistant rats and that it likely contributes to the postprandial alterations of glucose metabolism observed in the metabolic syndrome.
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PMID:Delayed insulin transport across endothelium in insulin-resistant JCR:LA-cp rats. 1090 90

Several clinical and metabolic abnormalities, i.e. central obesity, hypertension, impaired glucose tolerance or diabetes and dyslipidemia often cluster together and are commonly found in patients with atherosclerotic cardiovascular disease. Hyperinsulinemia and insulin resistance are often evident in subjects with these metabolic abnormalities, so called insulin resistance or metabolic syndrome. In the present study, we looked into the correlations between serum insulin or index of insulin sensitivity and various clinical and metabolic abnormalities. Subjects consisted of 103 males and 118 females. Oral glucose tolerance test was performed on all subjects. Homeostasis model assessment of insulin sensitivity (HOMA-S) was used to determine insulin sensitivity. In males, HOMA-S was found to be significantly correlated with BMI, plasma glucose, insulin, triglycerides and waist circumference. Male subjects in the highest quartile of HOMA-S also had significantly higher systolic blood pressure compared to those in the lowest quartile. In females, HOMA-S was significantly correlated with BMI, blood pressure, plasma glucose, insulin, triglycerides, HDL-cholesterol, waist circumferences and waist-hip ratio. However, after adjustment for BMI, correlation between HOMA-S and blood pressure in women was no longer statistically significant. We, therefore, concluded that correlations between serum insulin or index of insulin sensitivity with certain metabolic abnormalities also existed in Thai subjects. Some of these correlations seem to be at least in part dependent on obesity.
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PMID:Correlation between serum insulin and features of metabolic syndrome in Thais. 1093 14

Insulin resistance may cause a metabolic syndrome but whether insulin resistance causes hypertension is very controversial. Furthermore, it remains unclear whether the link between the insulin-resistance-related metabolic syndrome and hypertension is different between men and women. We examined fasting insulin, glucose, triglyceride and high-density lipoprotein (HDL)-cholesterol levels, systolic blood pressure, body mass index, and waist-to-hip ratio in a dataset from 8437 nondiabetic residents (age range, 30 to 89 years) in Kinmen. Factor analysis, a multivariate correlation statistical technique, was used to investigate the clustering and interdependence of these risk variables. Factor analysis identified two factors for men (n = 3659) and three factors for women (n = 4778, respectively. In men, a cluster of insulin, triglyceride, HDL-cholesterol, body mass index, and waist-to-hip ratio (metabolic syndrome) accounted for 29.7%, and a cluster of systolic blood pressure and glucose (hyperglycemia plus hypertension) accounted for 18.1% of the total variance in all variables considered. In women, a cluster of insulin, triglyceride, body mass index, waist-to-hip ratio, and systolic blood pressure (metabolic syndrome plus hypertension) accounted for 29.4%, a cluster of systolic blood pressure, glucose, and triglyceride (hyperglycemia plus hypertension plus dyslipidemia) accounted for 14.0%, and a cluster of triglyceride and HDL-cholesterol (dyslipidemia) accounted for 16.2% of the total variance. In conclusion, a distinct insulin-resistance-related metabolic syndrome characterized by hyperinsulinemia, dyslipidemia, and obesity was observed for both men and women in this Chinese population. However, hypertension was linked to the metabolic syndrome in women only.
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PMID:Different association of hypertension and insulin-related metabolic syndrome between men and women in 8437 nondiabetic Chinese. 1093 78

Insulin resistance (IR) is a phenomenon which associates several serious "diseases of civilization" within the framework of Reaven's metabolic syndrome. In the submitted paper the authors describe the so-called "paradox of insulin resistance"--a paradoxical finding of inadequate insulin action under laboratory induced conditions while under "common" conditions the finding is reversed. Diabetes mellitus type 2 (with obesity) is characterized by excessive filling of cells by energetically rich substances. A low energy output, inadequate physical activity in these subjects leads to the development of regulatory mechanisms, which restrict further nutrient (glucose) uptake from blood into cells. During subsequent stages of the disease the excessive glucose uptake by adipose tissue cells and muscle is ensured by the high concentration gradient, hyperglycaemia and hyperinsulinaemia. Induction of "comparable" conditions in clamp studies leads to paradoxical results. During relative hypoglycaemia and hypoinsulinaemia (as compared with normal conditions) the tissues of the diabetic patient, due to regulatory mechanisms, take up a smaller amount of glucose than tissues of non-diabetic subjects (although under normal conditions the glucose uptake is higher). This phenomenon is called "Paradox of insulin resistance". In a major proportion of patients IR can be induced by mere maintenance of hyperinsulinaemia, it can be minimalized by reducing the nutrient intake and by increasing physical exertion. Differentiation of patients where IR is a secondary, regulatory phenomenon is one of the basic tasks of the physician. Only patients who suffer from primary disorders of insulin function, primary IR and true insulin deficiency should be treated by administration of hyperinsulinaemia inducing drugs. It is questionable how suitable it is to administer these drugs to patients who suffer from a life-style disorder and are threatened by complications associated with hyperinsulinism.
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PMID:[The paradox of insulin resistance]. 1095 72

Sex hormone-binding globulin (SHBG) is a plasma glycoprotein with high binding affinity for testosterone and dihydrotestosterone and lower affinity for estradiol. SHBG is synthesized in the liver, and its plasma level is important in the regulation of plasma free and albumin-bound androgens and estrogens. Obesity and particularly excess visceral fat, known risk factors for cardiovascular and metabolic diseases, are associated with decreased testosterone levels in males and SHBG levels in both sexes. SHBG is usually positively correlated with high-density lipoprotein cholesterol and negatively correlated with triglyceride and insulin concentrations. A positive association between SHBG and various measures of insulin sensitivity has been demonstrated in both sexes, suggesting that decreased SHBG levels may be one of the components of the metabolic syndrome. We have examined pituitary-adrenocortical function, glucose tolerance, and lipoprotein and hormone levels in a large cohort of Finnish males. Abdominal obesity appears to be associated with slight hypocortisolemia and increased sensitivity to exogenous adrenocorticotropin stimulation, which may contribute to the hyperinsulinemia and related metabolic changes including decreased SHBG levels in males.
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PMID:Synthesis and regulation of sex hormone-binding globulin in obesity. 1099 12

In recent years, interest has tended to focus on prevention of coronary events in high-risk groups, particularly those with established coronary heart disease. While this is understandable, it has led to a lack of emphasis on primary prevention. Yet it is only by means of primary or even pri-mordial prevention that a substantial reduction in coronary mortality on a population level will be achieved. This becomes clear when we consider that half of all persons who suffer a first myocardial infarction will die within the first month thereafter. Nevertheless, major progress has been made in primary prevention. Reliable risk algorithms have been constructed in Europe (PROCAM) and the U.S., and preliminary analyses on both sides of the Atlantic indicate that these algorithms can be useful applied to populations which are geographically and ethnically distinct from those in which they were derived. A notable trend in recent years is the increasing recognition of the metabolic syndrome with its key components of abdominal obesity, hypertriglyceridemia hypertension, low HDL-C, small, dense LDL, insulin resistance and hyperinsulinemia as being perhaps the most common and dangerous metabolic abnormality of all. Newer risk markers are being evaluated. The position of homocysteine remains unclear. Despite a strong association of elevated homocysteine with risk in case-control studies, prospective investigations have been less convincing. Evidence is beginning to accumulate from cross-sectional and prospective studies that markers of inflammation such as C-reactive peptide may improve our ability to predict risk of coronary events. While these data are encouraging, results of further studies must be awaited before the true place of these markers can be determined. The same can be said of many genetic markers of risk. Though a very large number of association studies have indicated links between a variety of genetic markers and coronary risk, these effects have tended to disappear after controlling for epigenetic and confounding factors and with increasing sample sizes. Finally, much attention is being devoted to non-invasive imaging of the coronary arteries. Such methods hold much promise as a screening test to exclude coronary stenosis in low-risk individuals. However, the measurement of calcium content of the arterial wall by EBCT has yet to prove its usefulness as a predictor of coronary events.
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PMID:Primary prevention of coronary heart disease: from controversy to consensus. 1100 23


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