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

The association between type A behavior and a cluster of parameters of the metabolic syndrome was studied in 919 randomly selected healthy young adults. Type A behavior was measured using the Type A Behavior Questionnaire for the Finnish Multicenter Study and the Hunter Wolf A-B Rating Scale. The results showed that type A men scored higher on the "Metabolic Syndrome Precursors Factor," representing a metabolic entity, than did non-type A men. In addition, type A behavior had a moderating effect on the relationship between parameters of the metabolic syndrome, that is, interdependence of these somatic factors was stronger in type A men than in non-type A men. These findings were not true of women. It is discussed whether type A behavior might affect bodily functions through increased activity along the pituitary-adrenal system resulting in insulin resistance, compensatory hyperinsulinemia, and other characteristics of the metabolic syndrome.
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PMID:Type A behavior and metabolic syndrome precursors in young adults. 867 82

In this paper we presented characteristics of insulin resistance syndrome (IRS), also known as metabolic syndrome and syndrome X, with an emphasis on insulin resistance in hyperandrogenemic women. The aim features of IRS are obesity, hypertension, dyslipidemia-hypertriglyceridemia and decreased HDL cholesterol, impaired glucose tolerance with hyperinsulinemia and higher cardiovascular morbidity. It is considered typical that in hyperandrogenemia, especially in PCO syndrome, insulin resistance and hyperinsulinemia without other characteristics of IRS are expressed.
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PMID:[Androgen excess in women and the metabolic syndrome (syndrome X)]. 875 4

Survivors of childhood cancer have been reported to have a severalfold increased risk of death from cardiovascular disease. A cluster of metabolic abnormalities, including obesity, insulin resistance, hyperinsulinemia, glucose intolerance, hypertension, and dyslipidemia, have been designated as forming a metabolic syndrome that is associated with increased cardiovascular mortality. We studied 50 survivors (23 males) of childhood cancer, aged 10.5-31.2 yr, an average of 12.6 yr (range, 7.9-21.3 yr) after their diagnosis and compared them with 50 age- and sex-matched controls for signs of the metabolic syndrome by examining clinical and anthropometric measures, serum lipid profile, and fasting plasma insulin and glucose concentrations. Spontaneous nocturnal GH secretion was also evaluated in the cancer survivors. The patients had increased relative weight (P = 0.03) and body fat mass (P < 0.001), decreased serum high density lipoprotein (HDL) cholesterol (P < 0.001), and a reduced ratio of HDL to total cholesterol (P = 0.01). Fasting plasma glucose and insulin levels were higher (P < 0.001 and P = 0.003, respectively) in the cancer survivors than in the controls. The patients had an increased risk [odds ratio (OR), 4.5; 95% confidence interval (CI), 1.3-15.8; P = 0.01] of obesity (relative weight, > 120%), fasting hyperinsulinemia ( > 111 pmol/L; OR, 3.0; 95% CI, 1.0-8.6; P = 0.04), and reduced HDL cholesterol ( < 1.07 mmol/L; OR, 7.9; 95% CI, 2.2 to 29.6; P < 0.001). A combination of obesity, hyperinsulinemia, and low HDL cholesterol was seen in eight cancer survivors (16%), but in none of the controls (P = 0.01). This high risk group was characterized by reduced spontaneous GH secretion (P = 0.02). Long term survivors of childhood cancer appear to have an increased risk of manifestations of the metabolic syndrome. Decreased GH secretion may contribute to these metabolic abnormalities.
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PMID:Long-term survivors of childhood cancer have an increased risk of manifesting the metabolic syndrome. 876 73

Aging is associated with an increased incidence of hypertension, noninsulin-dependent diabetes mellitus, and coronary heart disease. Because these conditions often cluster in the same individuals, there has been speculation that a common mechanism is responsible for all of these pathological states. Both epidemiological and clinical research has shown that insulin resistance and/or hyperinsulinemia are associated with glucose intolerance, dyslipidemia (high plasma triglyceride and low high-density lipoprotein-cholesterol levels), and higher systolic and diastolic blood pressures. Therefore, insulin resistance and hyperinsulinemia have been proposed as the causal link among the elements of the cluster mentioned above, now most commonly referred to as the insulin resistance syndrome, syndrome X, or the metabolic syndrome. The elderly are more glucose intolerant and insulin-resistant, but it remains controversial whether this decrease in function is an inevitable consequence of "biological aging" or the result of what might be referred to as environmental or lifestyle variables: increased obesity, a detrimental pattern of fat distribution, or physical inactivity that usually accompany age. All of these modifiable environmental factors have also been shown to result in increases in insulin resistance and hyperinsulinemia and are risk factors for the development of the diseases of the metabolic syndrome. Recent interventional studies that have attempted to reverse these conditions in the elderly have shown improved insulin sensitivity, and glucose tolerance. Insulin secretion, on the other hand, seems to decrease with age even after adjustments for differences in adiposity, fat distribution, and physical activity. This may be responsible for the glucose intolerance in the very old even after improvements have been made in their lifestyle variables.
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PMID:The effect of age on insulin resistance and secretion: a review. 882 67

Rather than a link in a causal chain leading to hypertension, insulin resistance and resultant hyperinsulinemia may be 'spokes on a wheel', with central or visceral obesity as the postulated hub of the wheel. Hypertension, hypertriglyceridemia and high density lipoprotein cholesterol are depicted as other spokes. Newly identified metabolic pathways in adipose tissue or the modulating effects of various predisposing genes may lead to variable expression of various components of the multiple metabolic syndrome in individuals with a predisposition to the collection of visceral fat.
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PMID:Hypertension, dyslipidemia, and insulin resistance: links in a chain or spokes on a wheel? 888

Hypertension is associated with metabolic disturbances that may be related to hyperinsulinemia, both resulting from our lifestyle. Insulin resistance generated by central obesity, and complex relations with sympathetic activity, dyslipemia, atherosclerosis, sodium retention, altered vascular reactivity and hypertension, lead to pathophysiological connections, that are still to be understood. Even if obesity and hypertension were not related through hyperinsulinemia, the metabolic syndrome increases either vascular risk or hypertension, and it has to be re-evaluated whether essential hypertension is an adequate diagnosis for these patients.
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PMID:[Metabolic syndrome with vascular risk and arterial hypertension]. 893 72

In NIDDM a clustering of established coronary risk factors, e.g. the metabolic syndrome is responsible for excessive incidence of myocardial infarction. The harmful effects of these risk factors are aggravated by poor glucose control. Hyperinsulinaemia is associated with a higher level of risk factors for coronary heart disease. Individuals with subsequent myocardial infarction exhibit higher levels of serum insulin at entry. However, insulin in multivariate analysis was no independent risk factor. Perfect control of blood glucose, triglycerides and blood pressure was associated with a lower incidence of coronary heart disease. By extrapolation an integrated approach to correct the anomalies of the metabolic syndrome seems to be necessary to prevent macroangiopathy and improve life expectancy.
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PMID:Determinants for coronary heart disease in non-insulin-dependent diabetes mellitus: lessons from the diabetes intervention study. 896 95

Recent evidence suggests that insulin is mitogenic on the adrenal cortex and stimulates adrenocortical tumor formation. We, investigated whether hyperinsulinemia is present in 13 patients with incidentally detected adrenal tumors. Patients with adrenal incidentalomas were obese (mean BMI 29.7 +/- 1.2 kg/m2, normal < 25; % body fat 35 +/- 1.5%, normal < 30%) with increased abdominal fat deposition (waist to hip ratio 0.92 +/- 0.02, normal < 0.85). All 13 patients were insulin resistant. Five had NIDDM, of the remaining patients 5 had fasting insulin concentrations above 15 microE/ml, and all 8 patients had elevated insulin concentrations after 75 g of glucose orally. To further investigate the potential role of insulin we examined its effects on the NCI-h295 cell line. Insulin (1-100 micrograms/ml) stimulated cell proliferation in a time and dose-dependent matter without affecting cortisol synthesis. At this concentrations insulin was equally potent to IGF I (10-80 ng/ml) or IGF II (10-100 ng/ml). We conclude that the majority of patients with adrenal incidentalomas are insulin-resistant/hyperinsulinemic. Insulin stimulates adrenal cancer cell lines in vitro. We propose that adrenal incidentalomas are a newly recognized manifestation of the metabolic syndrome comparable to insulin-mediated stimulation of the ovary in the polycystic ovary syndrome.
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PMID:Adrenal incidentalomas: a manifestation of the metabolic syndrome? 896 38

A group of metabolic disorders including insulin resistance and hyperinsulinemia, impaired glucose tolerance, visceral obesity, hypertension, dyslipidemia, hyperuricemia, hypercoagulability and microalbuminuria determine the risk for the development of atherosclerosis, coronary artery disease and cerebral vascular disorders. Although available studies on the pathogenesis of the metabolic syndrome are equivocal, it is most frequently hypothesized that hereditary of insulin resistance leads to the remaining metabolic disorders including diabetes mellitus, atherosclerosis and coronary artery disease. Despite pathogenetic controversies, there are convincing arguments for the diagnosis of the metabolic syndrome and search for therapy improving insulin sensitivity and reducing hyperinsulinemia thus preventing the development of diabetes mellitus and coronary artery disease.
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PMID:[Insulin resistance and hyperinsulinemia--clinical aspects]. 899 30

Croatian Endocrine Society and Croatian Academy of Medical Sciences organized Symposium on Hyperandrogenaemia on March 22nd, 1996. Different aspects of this syndrome were discussed: epidemiology, classification and clinical features, steroid biosynthesis in the adrenal gland and ovarium, the genetics of polycystic ovarian syndrome (PCOS), clinical significance of testosterone and dihydrotestosterone metabolism, androgen excess and metabolic syndrome (syndrome X), insulin disturbances in PCOS, increased risk for development of non insulin dependent diabetes mellitus, androgen effects on serum lipoproteins, insulin like growth factors and function of ovarium, Doppler parameters in PCOS, treatment of hyperandrogenaemia, skin changes in PCOS, tests for adrenal and ovarial function, arterial hypertension and hyperinsulinism. National Board of Hyperandrogenaemia has been elected.
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PMID:[National consensus on hyperandrogenemia]. 901 36


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