Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A large segment of the population gradually develops insulin resistance, and the related metabolic syndrome is one of the most frequent causes of atherosclerosis. Searching for a practical indicator of insulin resistance, we studied the correlations between fasting serum insulin level, the general manifestations of insulin resistance syndrome, and various aspects of coronary artery disease in 797 men and 322 women. After we classified patients according to the quartiles of serum insulin level, we noted in the top quartile the presence of practically all manifestations of insulin resistance syndrome in persons of both sexes (e.g., increased waist/hip ratio, body mass index, glucose, uric acid, triglycerides, apolipoprotein B and decreased high-density lipoprotein cholesterol levels as well as apolipoprotein A-I/B ratios, and so forth). We also noted a higher prevalence of hypertension, diabetes mellitus, and type IV hyperlipidemia. Significantly more women in the fourth than in the first quartile had angiographically documented significant stenosis of the coronary arteries (p = 0.0016, odds ratio 2.9, 95% confidence interval 1.5 to 5.6) and previous myocardial infarction (p = 0.0297, odds ratio 2.1, 95% confidence interval 1.1 to 4.1). Men in both the first and the fourth quartile had a more disturbed lipid profile and a higher prevalence of significant stenoses of coronary arteries and/or previous myocardial infarction than women; there was a tendency toward a lower prevalence of alcohol consumption (p = 0.0503), a higher prevalence of gout (p = 0.0634), and previous myocardial infarction (p = 0.0791) in men in the fourth than in the first quartile.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Fasting hyperinsulinism, insulin resistance syndrome, and coronary artery disease in men and women. 748 1

Obesity is a remarkable heterogeneous condition as shown by the variety of metabolic complications encountered. Imaging techniques with computed tomography have made it possible to quantify adipose tissue deposited within the abdominal cavity (visceral fat) which has been found to be correlated with serum glucose, insulin and lipid levels. Individuals with excessive visceral fat have hypertriglyceridaemia, high apolipoprotein B levels and hypoalphalipoproteinaemia. Several genes could modulate the degree of dyslipidaemia in patients with excessive visceral fat. Consequently, these patients should be managed as a genetically identifiable subgroup at risk of developing metabolic complications of obesity. It would also be justified to focus treatment on mobilizing visceral fat and improving the metabolic syndrome rather than simply on weight loss, an often unrealistic and clinically unjustified objective.
 ...
PMID:[Grouping of risk factors for cardiovascular diseases in visceral obesity. Therapeutic implications]. 775 34

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.
 ...
PMID:Associations of fasting blood glucose with cholesterol absorption and synthesis in nondiabetic middle-aged men. 863 49

The author discusses metabolic processes during exogenous and endogenous lipid transport and deviations in the metabolism of lipids, lipoproteins and apolipoproteins in multiple metabolic syndrome and in so-called diabetic dyslipidaemia. Specific phenotypic manifestations of diabetic dyslipidaemia include hypertriacylglycerolaemia, hypercholesterolaemia, elevated plasma levels of LDL-cholesterol and apolipoprotein B and reduced levels of HDL-cholesterol and apolipoprotein B and reduced levels of HDL-cholesterol and apolipoprotein A-I. Other recent findings relating to this syndrome include evidence of elevated concentrations of small and dense LDL micelles (< 25 nm), so-called LDL phenotype B, which are easily modified (e.g. by oxidation, glycation etc.), and subsequent uptake by "scavenger" receptors into macrophages which after filling become foam cells and penetrate into the vascular wall. Elevated levels of small and dense LDL micelles, the accelerating process of atherogenesis, were proved in all multiple metabolic syndrome carriers. The atherogenic lipoprotein phenotype hastens markedly atherogenesis and subsequent manifestation of cardiovascular diseases.
 ...
PMID:[Genetic predisposition in multiple metabolic syndrome. Part 3. Metabolism of lipids, lipoproteins and apolipoproteins]. 1037 96

The current study assessed whether features of the metabolic syndrome are associated with higher apolipoprotein B(100) (apoB(100)) levels in people with Type 2 diabetes (n = 298) not taking lipid-lowering drugs. Body-mass index (BMI), waist:hip ratio (WHR), urinary albumin excretion rate, presence or absence of hypertension, uric acid levels, and apoB(100) levels were assessed. Both higher BMI and urinary albumin excretion rate were associated with higher apoB(100) levels (1.02 +/- 0.25 ( +/- S.D.) g/l in normal weight, 1.07 +/- 0.22 g/l in overweight and 1.14 +/- 0.25 g/l in obese individuals; P < 0.01; 1.09 +/- 0.23 g/l in normoalbuminuric patients, 1.06 +/- 0.22 g/l if urinary albumin excretion rate 20-50 microg/min and 1.17 +/- 0.27 g/l if urinary albumin excretion rate > 50 microg/min; P < 0.05). An association between the number of features of the metabolic syndrome and higher apoB(100) levels was found (1.03 +/- 0.22 g/l if no features, 1.08 +/- 0.25 g/l if one feature, 1.11 +/- 0.20 g/l if two features and 1.15 +/- 0.27 g/l if > 2 features; P for trend < 0.01). Thus apoB(100) levels show an association with the metabolic syndrome and, hypothetically, to insulin-insensitivity in Type 2 diabetes. BMI (but not WHR) and urinary albumin excretion rate accounted for most of the power of this relationship.
 ...
PMID:Relationships of apolipoprotein B(100) with the metabolic syndrome in Type 2 diabetes mellitus. 1212 70

Hyperandrogenemia and low levels of sex hormone binding globulin (SHBG) are frequently found in women with metabolic syndrome, which is characterized by low high-density lipoprotein cholesterol, hypertriglyceridemia, obesity, and hyperinsulinemia. The specific contribution of these various factors to coronary heart disease (CHD) is controversial. The coronary angiograms of 87 consecutive postmenopausal women were evaluated using 2 semiquantitative scoring systems to estimate the extent of focal and diffuse vessel wall alterations. Fasting sera were analyzed for levels of glucose, lipids, insulin, leptin, dehydroepiandrosterone sulfate, testosterone, and SHBG. Obesity was assessed by measuring body mass index, waist-to-hip ratio, skinfold thicknesses, and body impedance. After adjusting for age, there were significant differences in 55 women with CHD compared with 32 women without CHD: higher levels of low-density lipoprotein cholesterol (159 +/- 51 vs 132 +/- 39 mg/dl), apolipoprotein B (121 +/- 33 vs 102 +/- 29 mg/dl), triglycerides (115 vs 91 mg/dl), and basal insulin (7.5 vs 4.6 mU/L), as well as lower levels of high-density lipoprotein cholesterol (59.9 +/- 18.0 vs 69.0 +/- 17.1 mg/dl), SHBG (44.6 vs 68.1 nmol/L) and the quantitative insulin sensitivity check index (0.66 +/- 0.41 vs 0.93 +/- 0.73). Multivariate analysis by logistic regression identified age (odds ratio [OR] 1.22, 95% confidence intervals [CI] 1.09 to 1.37), smoking (OR 11.46, 95% CI 2.56 to 51.39), SHBG (OR 0.98, 95% CI 0.96 to 0.99), and apolipoprotein B (OR 1.02, 95% CI 1.01 to 1.04) as independently associated with the presence of CHD. Thus, low plasma levels of SHBG are associated with CHD in women independently of insulin, obesity markers, and dyslipidemia.
 ...
PMID:Relation of serum levels of sex hormone binding globulin to coronary heart disease in postmenopausal women. 1216 Dec 23

The growing epidemic of the metabolic syndrome is now well recognized and there is widespread effort to understand the pathogenesis of this complex syndrome and its major metabolic consequences. One of the severe complications accompanying insulin resistant states is the hypertriglyceridemia that appears to occur largely due to overproduction of triglyceride-rich, apolipoprotein B (apoB) containing-lipoproteins. As a result, mechanisms regulating the overproduction of these atherogenic apoB-containing lipoproteins have been the focus of much investigation in recent years. Both in vitro as well as in vivo models of insulin resistance are currently being used to further our understanding of the mechanisms involved in the deregulation of lipid metabolism in insulin resistant states. Evidence from these animal models as well as human studies has identified hepatic very low density lipoprotein (VLDL) overproduction as a critical underlying factor in the development of hypertriglyceridemia and metabolic dyslipidemia. In recent years, a dietary animal model of insulin resistance, the fructose-fed hamster model developed in our laboratory, has proven invaluable in studies of the link between development of an insulin resistant state, derangement of hepatic lipoprotein metabolism, and overproduction of apoB-containing lipoproteins. Evidence from the fructose-fed hamster model now indicates oversecretion of both hepatically-derived apoB100-containing VLDL as well as intestinal apoB48-containing triglyceride-rich lipoproteins in insulin resistant states. A number of novel intracellular factors that may be involved in modulation of VLDL have also been identified. This review focuses on these recent developments and examines the hypothesis that a complex interaction among enhanced flux of free fatty acids from peripheral tissues to liver and intestine, chronic up-regulation of de novo lipogenesis by hyperinsulinemia, and attenuated insulin signaling in the liver and the intestine may be critical to lipoprotein overproduction accompanying insulin resistance.
 ...
PMID:Mechanisms of metabolic dyslipidemia in insulin resistant states: deregulation of hepatic and intestinal lipoprotein secretion. 1245 12

The metabolic syndrome is characterized by insulin resistance and abnormal apolipoprotein AI (apoAI) and apolipoprotein B-100 (apoB) metabolism that may collectively accelerate atherosclerosis. The effects of atorvastatin (40 mg/day) and micronised fenofibrate (200 mg/day) on the kinetics of apoAI and apoB were investigated in a controlled cross-over trial of 11 dyslipidemic men with the metabolic syndrome. ApoAI and apoB kinetics were studied following intravenous d(3)-leucine administration using gas-chromatography mass spectrometry with data analyzed by compartmental modeling. Compared with placebo, atorvastatin significantly decreased (P < 0.001) plasma concentrations of cholesterol, triglyceride, LDL cholesterol, VLDL apoB, intermediate-density lipoprotein (IDL) apoB, and LDL apoB. Fenofibrate significantly decreased (P < 0.001) plasma triglyceride and VLDL apoB and elevated HDL(2) cholesterol (P < 0.001), HDL(3) cholesterol (P < 0.01), apoAI (P = 0.01), and apoAII (P < 0.001) concentrations, but it did not significantly alter LDL cholesterol. Atorvastatin significantly increased (P < 0.002) the fractional catabolic rate (FCR) of VLDL apoB, IDL apoB, and LDL apoB but did not affect the production of apoB in any lipoprotein fraction or in the turnover of apoAI. Fenofibrate significantly increased (P < 0.01) the FCR of VLDL, IDL, and LDL apoB but did not affect the production of VLDL apoB. Relative to placebo and atorvastatin, fenofibrate significantly increased the production (P < 0.001) and FCR (P = 0.016) of apoAI. Both agents significantly lowered plasma triglycerides and apoCIII concentrations, but only atorvastatin significantly lowered (P < 0.001) plasma cholesteryl ester transfer protein activity. Neither treatment altered insulin resistance. In conclusion, these differential effects of atorvastatin and fenofibrate on apoAI and apoB kinetics support the use of combination therapy for optimally regulating dyslipoproteinemia in the metabolic syndrome.
 ...
PMID:Differential regulation of lipoprotein kinetics by atorvastatin and fenofibrate in subjects with the metabolic syndrome. 1260 23

The constellation of risk factors known as the metabolic syndrome increases the risk of coronary artery disease at any low-density lipoprotein (LDL) cholesterol level. We performed an exploratory analysis of data from 5 trials to study the effects of rosuvastatin 10 mg on lipid levels and ratios in hypercholesterolemic patients (LDL cholesterol > or =160 mg/dL and <250 mg/dL) who met a modified National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) definition of the metabolic syndrome. Of 580 patients completing 12 weeks of treatment with rosuvastatin 10 mg, 194 (33%) met the definition of the metabolic syndrome by exhibiting > or =3 of the following: body mass index >30; triglycerides > or =150 mg/dL; high-density lipoprotein (HDL) cholesterol <40 mg/dL in men and <50 mg/dL in women; blood pressure > or =130/> or =85 mm Hg or receiving current medication for hypertension; and fasting blood glucose > or =110 mg/dL. Patients with the metabolic syndrome had higher triglyceride, non-HDL cholesterol, apolipoprotein B, and lipid ratios, and lower HDL cholesterol and apolipoprotein A-I levels, at baseline compared with patients without the metabolic syndrome. In patients with the metabolic syndrome, rosuvastatin 10 mg improved LDL cholesterol (-47%), non-HDL cholesterol (-43%), non-HDL cholesterol/HDL cholesterol ratio (-47%), apolipoprotein B (-37%), apolipoprotein B/apolipoprotein A-I ratio (-40%), triglycerides (-23%), apolipoprotein A-I (+7%), and HDL cholesterol (+10%)-in a manner similar to that in hypercholesterolemic patients who did not meet these criteria. Among patients who met the metabolic syndrome criteria and who had triglycerides > or =200 mg/dL, 64% met their ATP III non-HDL goals.
 ...
PMID:Efficacy of rosuvastatin 10 mg in patients with the metabolic syndrome. 1264 42

The objective of the present study was to examine concordance/discordance among 4 atherogenic indexes of cardiovascular risk: plasma total cholesterol, low-density lipoprotein (LDL) cholesterol, non-high-density lipoprotein (non-HDL) cholesterol, and apolipoprotein B-100 (apoB). Analyses were conducted in a cohort of 2,103 men without coronary artery disease (CAD) at the onset of the Quebec Cardiovascular Study. Although there were strong and highly significant correlations among the 4 risk indexes (0.78 < r < 0.97), only 50% of all subjects had concordant apoB and LDL cholesterol levels (i.e., values that fell into the same quintile of the population distribution). Moreover, concordance/discordance was not the same throughout the range of both variables; it was greater at the extremes of their respective distributions (65%), but significantly less in the midpoints (<40%). ApoB appeared to be more concordant with non-HDL cholesterol than with LDL cholesterol, although >1/3 of all subjects had discordant levels. Kappa analysis confirmed that there was only fair agreement between apoB and total or LDL cholesterol (0.38 and 0.36, respectively) and only moderate agreement between non-HDL cholesterol and apoB (0.47). Finally, a significant proportion of subjects (528 of 2,103) who had disproportionately higher apoB levels than would have been predicted based on their LDL cholesterol concentrations was more obese and manifested several features of the metabolic syndrome. They also had a significantly increased cardiovascular risk. In summary, plasma apoB and the various cholesterol indexes are complementary rather than competitive indexes of atherosclerotic risk and provide further evidence as to why measurement of apoB should be part of a standard lipoprotein assessment of CAD risk.
 ...
PMID:Concordance/discordance between plasma apolipoprotein B levels and the cholesterol indexes of atherosclerotic risk. 1274 98


1 2 3 4 5 6 7 8 9 10 Next >>