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

Primary hypertension is a frequent polygenic disease with strong genetic and environmental components. During the last decade, evidence has been increasing that insulin resistance as a marker of increased risk for Type 2 diabetes and cardiovascular atherosclerotic disease is present not only in individuals with obesity, Type 2 diabetes and impaired glucose tolerance, but also in the majority of the hypertensive population. Insulin resistance describes a tissue- and pathway-specific defect of glucose metabolism present in the so called 'metabolic syndrome'. Hyperinsulinaemia compensates for insulin resistance, leading to a cluster of undesirable processes predisposing to diabetes, atheroma and, directly or indirectly, hypertension. Candidate mechanisms whereby this metabolic syndrome might lead to hypertension include renal sodium retention, vascular hyperresponsiveness, arteriolar smooth muscle cell proliferation, altered cellular electrolyte transport and composition, stimulation of sympatho-adrenergic activity and growth promoting effects. Insulin per se does not appear to be the cause of elevated blood pressure as frequently seen in insulin-resistant states, but it may act with other factors to promote hypertension and atherosclerotic cardiovascular disease.
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PMID:New aspects of insulin resistance in hypertension. 799 75

The aim of this study was to investigate the pattern of body fat distribution and its association with metabolic and hormonal cardiovascular risk factors in women undergoing coronary angiography. Thirty of the 51 women exhibited significant coronary artery disease (CAD) (group A), whereas the remaining 21 subjects were free of major coronary stenoses (group B). Twenty-five healthy women without clinical signs of CAD served as a control group (group C). Despite comparable age and body mass index the women of group A had a significantly higher waist-to-hip ratio (WHR), a measure of the pattern of body fat distribution, than those of group C (0.88 +/- 0.07 vs. 0.78 +/- 0.06, P < 0.01). In an oral glucose tolerance test a high prevalence of impaired glucose tolerance or diabetes was found in groups A and B (53% and 63%, respectively) compared with group C (4%, each P < 0.01). The women of groups A and B showed significantly higher blood pressure and triglyceride levels as well as lower HDL-cholesterol than those of group C, whereas total and LDL-cholesterol were not different between the groups. The serum concentrations of testosterone, sex-hormone-binding globulin (SHBG) and cortisol were comparable between the three groups and correlation analysis revealed positive associations between androgens and WHR (r = 0.36, P < 0.01) and serum insulin (r = 0.34, P < 0.01) respectively. These findings indicate that women with angiographically confirmed CAD, and those with clinical signs of CAD but without significant stenosis, frequently exhibit a metabolic syndrome characterized by a cluster of metabolic abnormalities which may underlie the atherosclerotic process.
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PMID:Body fat distribution and its association with metabolic and hormonal risk factors in women with angiographically assessed coronary artery disease. Evidence for the presence of a metabolic syndrome. 800 97

We have investigated the prevalence of cardiovascular risk factors including insulin and lipoprotein(a) in 40-year old men from the island of Oland (n = 314, 84% of those invited) in order to assess to what extent insulin and lipoprotein(a)--two of the currently discussed risk factors--correlated with each other, as well as with some of the more established risk factors. An inverse correlation was found in bivariate analyses between lipoprotein(a) and some of the risk factors for cardiovascular disease included in the 'metabolic syndrome' (triglycerides; r = -0.15, BMI; r = -0.18, and insulin/glucose ratio; r = -0.18) (p < 0.001). In multivariate analysis only the inverse correlation with triglycerides remained. Since lipoprotein(a) has been shown to be an independent risk factor for myocardial infarction, there may exist two subgroups of cardiovascular risk patients: one more obese, hyperinsulinaemic and with several metabolic derangements; and another comprising non-obese subjects with higher lipoprotein(a) values.
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PMID:Non-obese men with high lipoprotein(a) values--a cardiovascular risk group different from those with the metabolic syndrome? 819 5

The associates of gout-obesity, hypertriglyceridemia, glucose intolerance, and hypertension, strikingly resemble those of insulin resistance. In the present study we determined whether hyperuricemia is associated with insulin resistance and, if so, whether this association can be explained by other components of the syndrome. For this purpose we quantitated insulin sensitivity (euglycemic clamp) in 37 nondiabetic subjects (aged 30-68 yr) exhibiting varying degrees of the metabolic syndrome (body mass index, 21.5-35.7 kg/m2; serum triglycerides, 0.4-22.0 mmol/L; high density lipoprotein cholesterol 0.38-1.86 mmol/L; blood pressure, 190-100/116-60 mm Hg). In simple linear regression analysis, the serum uric acid concentration (range, 182-568 mumol/L) was inversely correlated with insulin sensitivity (rate of glucose utilization; r = -0.61; P < 0.001) and positively with serum triglycerides (r = 0.68; P < 0.001), but not with body mass index, age, or the plasma glucose concentration. In multiple linear regression analysis, both insulin sensitivity (P < 0.05) and serum triglycerides (P < 0.005) were independently associated with the serum uric acid concentration, and together explained 50% of its variation. Addition of body mass index or age to the model did not improve the degree of explanation. Acute elevation of serum triglycerides about 3-fold, of plasma FFA about 9-fold, or of serum insulin about 28-fold had no effect on the serum uric acid concentration in healthy volunteers. The data indicate that hyperuricemia is indeed an inherent component of the metabolic syndrome and could also be used as a simple marker of insulin resistance.
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PMID:Hyperuricemia and insulin resistance. 828 9

NIDDM has been postulated to be a component of a more generalized metabolic syndrome, Syndrome X, caused by insulin resistance. Although the components of the syndrome include glucose intolerance, hypertension, increased TG, and decreased HDL cholesterol, their relationship to insulin resistance and/or hyperinsulinemia is controversial. Recent investigations have shown racial differences in the relationship between insulin resistance and BP in nondiabetic populations. We assessed the relationship between insulin resistance and the other components of the syndrome in 37 black men and 53 black women with NIDDM. Insulin sensitivity was determined by measuring glucose disposal with the euglycemic insulin clamp technique with a 1 mU.kg-1.min-1 insulin infusion. We also determined fasting lipid profiles and BP. In this group of black men and women with NIDDM, 30% were insulin sensitive, and 70% were insulin resistant. No correlation existed between insulin sensitivity and sBP or dBP in either sex. Fasting serum TGs were inversely correlated with insulin sensitivity for both men (r = -0.401, P = 0.02) and women (r = -0.366, P = 0.008). Serum HDL cholesterol was highly correlated with insulin sensitivity for men (r = 0.421, P = 0.01) but not for women (r = 0.071, P = 0.62). Fasting serum TG levels and serum HDL-cholesterol levels were highly correlated in an inverse relationship in men (r = -0.368, P = 0.03), but not women (r = -0.199, P = 0.17). In summary, BP does not correlate with insulin resistance in blacks with NIDDM. Normal insulin sensitivity occurs in 33% of black men and 25% of black women with NIDDM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Do blacks with NIDDM have an insulin-resistance syndrome? 843 15

The occurrence of multi-metabolic syndrome was studied by authors on 31 patients with obesity of android type and hypertension. Plasma glucose and plasma insulin levels were investigated during oral glucose tolerance test, plasma lipid levels were determined, furthermore body mass index and waist/hip ratio were calculated. It was considered that in 65 percent of the cases the presence of multi-metabolic syndrome could have been proved. Dyslipidemia in 22 cases, hyperinsulinemia in 20 cases, deterioration of the carbohydrate metabolism in 14 cases could be demonstrated. The negative correlation between glucose- and insulin-responses to glucose challenge may suggest the presence of insulin resistance. No significant difference was found in metabolic parameters between men and women. The multi-metabolic syndrome is regarded by authors as a process which may lead to both type 2 diabetes mellitus and atherosclerosis. According to their appearance about two third of these patients could be screened. Authors emphasize the great significance of this problem and the importance of early diagnosis and prevention.
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PMID:[Hypertension and multimetabolic syndrome]. 844 28

The treatment of type II diabetes should not only concentrate on blood glucose levels but also should take symptoms like insulin resistance, hyperinsulinemia, low HDL-cholesterol, high VLDL, and systemic hypertension into consideration. These symptoms are well described by the metabolic syndrome and are known to be risk factors of macroangiopathy. In obese type II diabetic patients weight loss by caloric restriction is the most essential therapeutic step. Retarding intestinal carbohydrate uptake glucosidase-inhibitors are able to lower postprandial blood glucose levels without stimulating insulin secretion. The biguanide metformin is suitable to diminish peripheral insulin resistance, gluconeogenesis, and intestinal glucose absorption on cellular mechanisms others than betacytotropic effects. In non obese type II diabetic patients sulfonylureas are advantageous because of meal related stimulation of endogenous insulin which runs the physiological way with first pass through the liver. Therefore, sulfonylurea treatment should be continued when secondary failure indicates the need for exogenous insulin. In accordance with the course of type II diabetes in secondary failure insulin should be added to sulfonylureas in as small amounts as possible to ameliorate poor metabolic control. Thus iatrogenic hyperinsulinemia and resulting insulin resistance can be largely avoided. If there is any long term benefit when different oral antidiabetic agents are administered together with insulin has to be evaluated in further clinical studies.
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PMID:[Combination therapy of oral antidiabetic drugs with insulin]. 847 36

Relationships between cardiovascular risk factors, body composition, and tissue distributions were examined in 10 Indian and 10 Swedish males matched by age, height, and weight. The body was divided into 29 compartments by means of a multiscan computed tomography (CT) technique. Fasting glucose, insulin, and triglycerides (TG) were higher in Indians than in Swedes. During the oral glucose tolerance test (OGTT), the glucose area was similar in both groups, whereas the insulin area was 80% larger in Indians. Adipose tissue (AT) and skin volumes were larger and remaining lean tissues were smaller in Indians. Indians had proportionally less muscle and more skeleton in the legs, but no ethnic difference could be demonstrated with respect to AT distribution. The visceral AT to total AT volume ratio was positively related to insulin and TG, and with higher risk factors for Indians at any given ratio. TG and glucose were negatively related to the leg muscle to total muscle volume ratio, and this ratio was smaller in Indians. It is concluded that the metabolic disturbances of Indians are not necessarily dependent on a preponderance of visceral AT, and also that an upper-body muscle distribution-recognized as a new phenotypic companion to the metabolic syndrome-is statistically related to cardiovascular risk factors.
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PMID:Computed tomography-determined body composition in relation to cardiovascular risk factors in Indian and matched Swedish males. 862 9

NIDDM and the metabolic syndrome are characterized by a low serum, HDL cholesterol content and a high triglyceride level, whereas total and LDL cholesterol concentrations are not necessarily elevated. Variable results have been reported on cholesterol absorption, elimination, and synthesis in NIDDM, but no studies are available on subjects within the normal range of blood glucose. From serum samples collected in 1985 from 203 nondiabetic men aged 51-66 years, we examined lipids, cholesterol precursors (reflecting cholesterol synthesis), and plant sterols and cholestanol (reflecting cholesterol absorption) in relation to fasting blood glucose. The findings prompted us (in 1993) to further examine 11 men from the highest and lowest glucose thirds of 203 nondiabetic men by additional dietary, serum, and fecal analyses for absorption, elimination, and synthesis of cholesterol and insulin sensitivity. In 1985, blood glucose was significantly related to LDL apolipoprotein B (P = 0.05) but not to LDL cholesterol (P = 0.19). Significantly higher serum lathosterol and desmosterol-to-cholesterol proportions and lower plant sterol and cholestanol proportions in the highest rather than the lowest glucose thirds suggested that the subjects with high normal blood glucose had decreased absorption and enhanced synthesis of cholesterol. In 1993, men with the lowest glucose versus those with the highest glucose had a lower waist-to-hip ratio, plasma HbA1c, fasting and postload insulin and glucose values, and a higher insulin sensitivity index. In agreement with the 1985 non-cholesterol sterol data, direct analyses of cholesterol metabolism showed further higher cholesterol absorption efficiency (P = 0.03) and serum plant sterol and cholestanol proportions (P < 0.001). Despite a slightly lower dietary cholesterol intake, cholesterol synthesis (P = 0.02) and serum lathosterol (P < 0.01) and desmosterol (P < 0.01) proportions were lowest in men with the lowest glucose third. We conclude that noncholesterol sterols in serum exhibits a long-lasting correlation with blood glucose level in a nondiabetic male population. Low intestinal absorption and high synthesis of cholesterol characterize men with high normal blood glucose. Differences in cholesterol metabolism could be due to underlying insulin effects associated with obesity-like fat distribution and may thus imply novel aspects in the metabolic interrelation between insulin and cholesterol in humans.
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PMID:Associations of fasting blood glucose with cholesterol absorption and synthesis in nondiabetic middle-aged men. 863 49

For better comprehension of the metabolic syndrome, it is necessary to differentiate the effect of insulin on glucose metabolism on the one hand, and on other metabolic activities on the other hand. Whereas glucose utilization is affected by insulin resistance, the effect of insulin on lipid metabolism, ion and aminoacid transport does not seem to be diminished. Lipid metabolism, however, seems to play a crucial role in the induction of the vicious cycle. Increased energy and fat ingestion may be due to an increased number of galanin secreting cells in the hypothalamus. The excessive fat intake results in an increased rate of release of insulin and increased influx of triglycerides into the blood. From these triglycerides an excess of free fatty acids is released by the action of lipoprotein lipase. The increased plasma free fatty acid level then results in insulin resistance affecting glucose metabolism. Also, these free fatty acids may impair the secretion of insulin. Induction of insulin resistance results in higher glucose levels, which may cause hyperinsulinemia. Hyperinsulinemia maintains the elevation of triglycerides. When diabetes becomes overt and elevated glucose levels prevail, the hyperinsulinism acts on the metabolic pathways which are still sensitive to insulin, namely lipid metabolism, aminoacid transport and ion transport.
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PMID:Hyperinsulinemia, hyperproinsulinemia and insulin resistance in the metabolic syndrome. 864 79


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