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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)
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PMID:Fasting hyperinsulinism, insulin resistance syndrome, and coronary artery disease in men and women. 748 1

We investigated the association between fasting insulin concentration--an indicator of insulin resistance in nondiabetic individuals--cardiovascular risk factors, and coronary heart disease in a study of 390 men in the town of Zutphen. In 1990, an extensive examination was carried out on the participating men (aged 70 to 89 years). Fasting insulin levels were determined and a number of other risk factors measured. Known and newly diagnosed diabetics were excluded from the data analyses. Fasting insulin concentration was significantly associated with levels of glucose, triglycerides, uric acid, serum albumin, creatinine, and fibrinogen as well as resting heart rate. Inverse associations with high-density lipoprotein cholesterol and factor VII activity were observed. These results were independent of confounding factors such as age, body mass index, ratio of subscapular to triceps skinfold thicknesses, cigarette smoking, physical activity, and alcohol consumption. Men with a fasting insulin level higher than 80 pmol/L (highest quartile of the distribution) had a significantly higher prevalence of coronary heart disease and especially of myocardial infarction. This result was independent of potential confounding variables as well as of possible intermediates (total and high-density lipoprotein cholesterol, hypertension, serum triglycerides, fasting glucose, and other risk factors related to fasting insulin) (odds ratio, 2.2; 95% confidence interval, 1.2-4.0). No association between fasting insulin level and hypertension or blood pressure was observed. These results show that fasting insulin is an important indicator of coronary heart disease in elderly men. Clotting factors, resting heart rate, uric acid, serum albumin, and creatinine may also play a role in this metabolic syndrome.
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PMID:Hyperinsulinemia, risk factors, and coronary heart disease. The Zutphen Elderly Study. 791 15

The purpose of this study was to test the hypothesis of a causal relationship between high insulin levels and the development of benign prostatic hyperplasia (BPH) and to determine the clinical, anthropometric, metabolic and insulin profile in men with fast-growing BPH compared with men with slow-growing BPH. The present study was designed as a risk factor analysis of BPH in which the estimated annual BPH growth rate was related to components of the metabolic syndrome. Two hundred and fifty patients referred to the Urological Section, Department of Surgery, Central Hospital, Varberg, Sweden, with lower urinary tract symptoms with or without manifestations of the metabolic syndrome were consecutively included. The prevalences of atherosclerotic disease manifestations, non-insulin-dependent diabetes mellitus (NIDDM) and treated hypertension were obtained. Data on blood pressure, waist and hip measurement, body height and weight were collected and body mass index (BMI) and waist/hip ratio (WHR) were calculated. Blood samples were drawn from fasting patients to determine insulin, total cholesterol, triglycerides, HDL and LDL cholesterol, uric acid, alanine aminotransferase (ALAT) and prostate-specific antigen (PSA). The prostate gland volume was determined using ultrasound. The median annual BPH growth rate was 1.04 ml/year. Men with fast-growing BPH had a higher prevalence of NIDDM (p = 0.023) and treated hypertension (p = 0.049). These patients were also taller (p=0.004) and more obese as measured by body weight (p<0.001), BMI (p=0.026), waist measurement (p <0.001), hip measurement (p = 0.006) and WHR (p=0.029). Moreover, they had elevated fasting plasma insulin levels (p = 0.018) and lower HDL cholesterol levels (p = 0.021) than men with slow-growing BPH. The annual BPH growth rate correlated positively with diastolic blood pressure (rs = 0.14; p = 0.009), BMI (rs = 0.24; p < 0.001) and four other expressions of obesity and fasting plasma insulin level (rs = 0.18; p = 0.008), and negatively with the HDL cholesterol level (rs = -0.22; p = 0.001). In conclusion, the data suggest that NIDDM, hypertension, tallness, obesity, high insulin and low HDL cholesterol levels constitute risk factors for the development of BPH. The results also suggest that BPH is a component of the metabolic syndrome and that BPH patients may share the same metabolic abnormality of a defective insulin-mediated glucose uptake and secondary hyperinsulinaemia, as patients with the metabolic syndrome. The findings support the hypothesis of a causal relationship between high insulin levels and the development of BPH, and give rise to a hypothesis of increased sympathetic nerve activity in men with BPH.
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PMID:Clinical, anthropometric, metabolic and insulin profile of men with fast annual growth rates of benign prostatic hyperplasia. 1041 80

It has been suggested that increased activity of the hypothalamic-pituitary-adrenal axis may link low birth weight with subsequent development of cardiovascular risk factors and disease. Two hundred and five men, aged 66-77 yr, who were born and still live in East Hertfordshire underwent an overnight very low dose (0.25 mg) dexamethasone suppression test followed by a low dose 1-microgram ACTH-(1-24) stimulation test. A 24-h urine sample was collected for analysis of cortisol metabolites by gas chromatography/electron impact mass spectrometry. Men with lower birth weight had enhanced responses of plasma cortisol to ACTH-(1-24) (P = 0.03), increased total urinary cortisol metabolite excretion (after adjustment for confounding effects of increased obesity and lean body mass in high birth weight men; P = 0.04), but no difference in plasma cortisol after dexamethasone. Features of the metabolic syndrome were independently associated with enhanced adrenal responsiveness to ACTH-(1-24) (raised blood pressure, P = 0.02; glucose intolerance, P = 0.09; hypertriglyceridemia, P = 0.02), with trends to increased urinary cortisol metabolite excretion, but not with differences in plasma cortisol after dexamethasone. Men with low birth weight and/or the metabolic syndrome have increased activity of the hypothalamic-pituitary-adrenal axis. This may be an important mechanism underpinning the effects of events in early life on later cardiovascular disease.
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PMID:Altered control of cortisol secretion in adult men with low birth weight and cardiovascular risk factors. 1123 8

Impaired fasting glucose (fasting plasma glucose 6.1 to 6.9 mmol/L [110 to 125 mg/dL]) is a common glycemic disorder which usually progress to diabetes mellitus. The relationships between impaired fasting glucose, other risk factors including blood pressure, and mortality have never been clearly investigated. We studied 63 443 consecutive men (ages 21 to 60 years), each of whom had a routine health examination with a fasting plasma glucose measurement. Men with known ischemic cardiac disease and treatment for diabetes or hypertension were excluded. Impaired fasting glucose was found in 10 773 (17.0%) of these men. Mean body mass index, serum triglyceride and cholesterol levels, and systolic, diastolic, and pulse blood pressure were significantly higher for men with impaired fasting glucose compared with those men with normal fasting glucose (fasting plasma glucose 3.9 to 6.0 mmol/L). When adjusted for confounding variables, relative risk of 8-year cardiovascular mortality associated with impaired fasting glucose was dependent on systolic blood pressure level (1.02 [95% CI: 0.62 to 1.70] when <140 mm Hg and 2.10 [95% CI: 1.16 to 3.80] between 140 and 160 mm Hg). Inversely, relative risk of 8-year cardiovascular mortality associated with moderate systolic hypertension (140 to 159 mm Hg) compared with normal systolic blood pressure (<140 mm Hg) was highly dependent on the glycemic status (2.97 [95% CI: 1.58 to 5.55] for men with impaired fasting glucose compared with 1.35 [95% CI: 0.84 to 2.18] in those with normal fasting glucose). Similar results were found concerning overall mortality. In conclusion, the presence of moderate systolic hypertension can identify subjects with impaired fasting glucose who are at risk of cardiovascular and overall mortality, and vice versa, probably through the metabolic syndrome.
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PMID:Impaired fasting glucose, blood pressure and cardiovascular disease mortality. 1236 47

The relationships between alcohol consumption, serum gamma-glutamyltransferase (GGT) levels, and the prevalence of major coronary risk factors were analyzed cross-sectionally in 2,399 male and 1,402 female middle-aged workers, to clarify the effects of moderate alcohol consumption on the development of the metabolic syndrome. Male moderate drinkers, consuming less than 60 ml of alcohol per day, had a lower prevalence of upper body obesity and low serum HDL-cholesterolemia (LHDLC) in comparison with nondrinkers, but not of hypertension, impaired glucose tolerance or hypertriglyceridemia (HTG). In women, alcohol consumption did not show any significant associations with the coronary risk factors. Men with an elevated serum GGT (EGGT) of 40 U/l or above had a significantly higher odds ratio for all the coronary risk factors as compared with those with normal GGT, even after adjusting for alcohol consumption, together with age, body mass index, cigarette consumption and physical activity. Women with an EGGT of 25 U/l or above had similar findings, although significance was found only in HTG. Nearly 80% and 55% of the appearance of EGGT in men and women were attributable to alcohol consumption, and 20% and 10% of the male and female moderate drinkers had EGGT. These results suggest that even moderate alcohol consumption will increase coronary risk factors characteristic of the metabolic syndrome in drinkers who have an increase in serum GGT. Further studies are required to confirm the causal association between alcohol consumption, increase in serum GGT and development of the metabolic syndrome.
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PMID:Alcohol consumption, serum gamma-glutamyltransferase levels, and coronary risk factors in a middle-aged occupational population. 1464 70

Development of hypertension has been linked to chronic low-grade inflammation. However, it is not known whether this connection is mediated by features of the metabolic syndrome or smoking, or their changes, which themselves have been linked to inflammation. We studied the predictive value of highly sensitive C-reactive protein (hs-CRP), smoking, and abdominal obesity to the development of hypertension in an 11-year follow-up of a population-based study cohort comprising 379 middle-aged normotensive men. During the follow-up, 124 men (33%) developed hypertension. Men with hs-CRP > or =3.0 mg/L were 2.8x (95% confidence interval, 1.2 to 6.6) more likely to develop hypertension than with hs-CRP <1.0 mg/L even after adjustment for features of the metabolic syndrome, lifestyle factors, and their changes. Cigarette smoking was also associated with development of hypertension independently of inflammation and other confounders. Waist girth increased more in men who quit smoking than in other men. An increase in waist girth during follow-up strongly predicted incident hypertension. The decrease in smoking was not associated with a lower risk of hypertension in age-adjusted analyses. Hypertension is preceded by low-grade chronic inflammation in middle-aged white men independently of smoking or features of the metabolic syndrome. Furthermore, smoking may be a risk factor for hypertension. Although stopping smoking is beneficial with respect to health outcomes, the subsequent increase in weight and waist girth associated with smoking cessation may offset the decrease in the risk of hypertension that one may otherwise expect.
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PMID:Inflammation, abdominal obesity, and smoking as predictors of hypertension. 1549 31

Low rates of fetal and infant growth are associated with the metabolic syndrome and cardiovascular disease in later life. We investigated common genetic variation in the GH-CSH gene cluster on chromosome 17q23 encoding GH, placental lactogens [chorionic somatomammotropins (CSH)], and placental GH variant in relation to fetal and infant growth and phenotypic features of the metabolic syndrome in subjects aged 59-72 yr from Hertfordshire, UK. Allele groups T, D1, and D2 of a locus herein designated CSH1.01 were examined in relation to GH-CSH single nucleotide polymorphisms and to specific phenotypes. Average birth weights were similar for all genotype groups. Men with T alleles were significantly lighter at 1 yr of age, shorter as adults, and had higher blood pressures, fasting insulin (T/T 66% higher than D2/D2) and triglyceride concentrations, and insulin and glucose concentrations during a glucose tolerance test. Birth weight and 1-yr weight associations with metabolic syndrome traits were independent of the CSH1.01 effects. Common diversity in GH-CSH correlates with low 1-yr weight and with features of the metabolic syndrome in later life. GH-CSH genotype adds substantially to, but does not account for, the associations between low body weight, at birth and in infancy, and the metabolic syndrome.
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PMID:Late life metabolic syndrome, early growth, and common polymorphism in the growth hormone and placental lactogen gene cluster. 1553 13

In men, hypoandrogenism is associated with features of the metabolic syndrome. It is not known whether men with the metabolic syndrome are at a higher risk of developing hypogonadism. We therefore assessed whether the metabolic syndrome predicts development of hypogonadism 11 yr later in 651 middle-aged Finnish men participating in a population-based cohort study. Men with the metabolic syndrome at baseline as defined by the World Health Organization (n = 114, 20%) had a 2.6-fold increased risk of developing hypogonadism as defined by total testosterone levels less than 11 nmol/liter at the 11-yr follow-up independent of age, smoking, and other potential confounders. Further adjustment for body mass index (OR, 2.0; 95% CI, 1.1-3.8) or baseline total testosterone levels (OR, 1.9; 95% CI, 1.0-3.4) attenuated the association. The association of the metabolic syndrome with hypogonadism as defined by calculated free testosterone levels less than 225 pmol/liter was similar, but weaker. The adjusted decrease in testosterone concentrations during the 11-yr follow-up was also greater in men with than without the metabolic syndrome. Smokers had a nonsignificantly lower risk of developing hypogonadism during follow-up, whereas a decrease in smoking increased the risk of hypogonadism. The metabolic syndrome predisposes to development of hypogonadism in middle-aged men. Prevention of abdominal obesity and the accompanying metabolic syndrome in middle age may decrease the risk of hypogonadism in men, especially in those who quit smoking.
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PMID:The metabolic syndrome and smoking in relation to hypogonadism in middle-aged men: a prospective cohort study. 1553 58

Relatively limited contemporary information is available about the magnitude of, and factors associated with, the metabolic syndrome in adult men and women. The purpose of our observational study was to describe the prevalence and predictors of the metabolic syndrome in a sample of employed adults attending a worksite cardiovascular screening program. The study sample consisted of 871 men and women between the ages of 21 and 77 years from 6 locations of the parent company. These individuals attended an employer-sponsored cardiovascular screening and wellness program during 2003. A standardized questionnaire was administered to all study participants and a number of different coronary risk factors were measured. Approximately 27% of the study sample was classified as having the metabolic syndrome. Men, persons with a history of hypertension, heart disease, or stroke, sedentary individuals, and those with an increased heart rate and higher levels of C-reactive protein were associated with presence of the metabolic syndrome. A relatively similar risk factor profile was noted in persons without a self-reported history of prior cardiovascular disease. The results of our cross-sectional observational study suggest that the prevalence of the metabolic syndrome is considerable. A number of demographic, comorbid, and other factors are associated with this syndrome. Increased attention to the metabolic syndrome, and modification of predisposing factors, remains of considerable public health and clinical importance.
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PMID:Metabolic syndrome in a screened worksite sample: prevalence and predictors. 1566 35


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