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

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

Considerable progress has been made in our understanding of the role of the nervous system in human hypertension. The evidence for a widespread autonomic abnormality in the early phases of hypertension is overwhelming and excessive sympathetic activity is consistently present in such patients since their childhood. The enhanced sympathetic tone in hypertension is associated with the metabolic syndrome of insulin resistance and dyslipidemia. Multiple mechanisms by which sympathetic overactivity could cause both hypertension and the metabolic syndrome have been documented. Furthermore, the excessive sympathetic tone is conducive to coronary heart disease through its association with high hematocrit values and with excessive platelet aggregability. Surprisingly, the myth that patients with neurogenic hypertension have a benign prognosis continues to persist. Much of the misunderstanding stems from the idea that patients with neurogenic hypertension, commonly called "white coat" or borderline hypertension, do not develop established hypertension. There is no support for such an assessment; in fact, patients with neurogenic hypertension are at a high risk of future accelerated hypertension. Another misunderstanding relates to differences in hemodynamics between neurogenic and established hypertension. It is true that patients with neurogenic hypertension initially show an increase of cardiac output. However, this later evolves into a classic picture of established high resistance hypertension. The hemodynamic transition is secondary to a decrease in cardiac responsiveness and an increase in vascular responsiveness over the course of hypertension. With passage of time, vascular reactivity increases, yet sympathetic tone tends to decrease. This can be explained by the "blood pressure seeking behavior of the central nervous system." In hypertension, the central nervous system appears to seek a higher blood pressure level and, as the vasculature becomes hyperresponsive, less sympathetic tone is needed to maintain the elevated blood pressure. This decrease of sympathetic tone in later phases of hypertension should not be viewed as a normalization, since sympathetic tone in relationship to vascular hyperresponsiveness remains excessive and the central nervous system maintains a crucial role in sustaining high blood pressure in hypertension.
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PMID:Sympathetic overactivity in hypertension. A moving target. 893 44

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

The 10-year follow-up of the Munich General Practitioner Project was designed as a long-term prospective study to evaluate factors predicting macrovascular and overall mortality in a random cohort of non-insulin-dependent diabetic (NIDDM) patients. Of the original 290 patients (103 males, 187 females, median age 65 years) 92.5% could be assessed, 103 subjects had died, 58 from macrovascular causes. In an univariate analysis of baseline data, deceased patients, and especially those who died from macrovascular causes had significantly higher fasting blood glucose, HbA1c, von Willebrand-factor protein, urine albumin excretion, and serum beta 2-microglobulin, were significantly older, exhibited significantly more ischaemic heart disease (abnormal ECG Minnesota codes), carotid artery and peripheral vascular disease (both determined by ultrasound-Doppler), and had significantly inferior knowledge about diabetes and its treatment. No significant differences were seen for gender, blood pressure, smoking, total cholesterol, triglycerides, HDL-cholesterol, or the use of antidiabetic, antihypertensive or coronary drugs. In a multiple logistic regression analysis, the risk factors for macrovascular death were age, HbA1c and von Willebrand-factor protein. When baseline macrovascular disease was taken into account, carotid artery disease was also a determinant. The main variables from the metabolic syndrome (blood pressure, dyslipidaemia, body mass index) did not enter a multiple logistic regression analysis. The data suggest that age and haemoglobin A1c are major determinants, and that in addition von Willebrand-factor associated endothelial damage is a risk factor for macrovascular mortality in NIDDM patients.
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PMID:Predictors of 10-year macrovascular and overall mortality in patients with NIDDM: the Munich General Practitioner Project. 896 Aug 40

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

Recently, an inverse correlation between serum uric acid concentrations and insulin sensitivity has been described in subjects with varying degrees of metabolic syndrome, suggesting that measurement of serum uric acid may provide a simple marker of insulin resistance. Several biochemical and clinical features of polycystic ovary syndrome (PCOS) resemble those of metabolic syndrome: women with PCOS are often obese; they are also at increased risk for the development of coronary artery disease, hypertension and diabetes mellitus. The objective of the present study was to analyse the usefulness of serum uric acid measurement in screening for the metabolic syndrome in women with PCOS. For that purpose serum concentrations of uric acid, insulin and triglycerides were measured in 38 women with PCOS and 20 weight-matched control women with regular menstrual cycles. No differences were found in the uric acid concentrations between the PCOS and control groups. The mean concentrations of triglycerides and fasting insulin were higher in the women with PCOS than in the healthy controls. Serum uric acid concentrations were inversely related to serum hormone-binding globulin (SHBG) concentrations, and positively with body mass index (BMI), insulin concentrations and testosterone:SHBG ratio in the PCOS group. Our results suggest that measurement of serum uric acid does not provide new means for identification of metabolic syndrome in patients with PCOS.
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PMID:Normal serum uric acid concentrations in women with polycystic ovary syndrome. 898 Nov 20

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

Metabolic syndrome is characterized by a large number of metabolic disorders, the findings being generally a combination of insulin resistance, obesity, hypertension, dislipidemia and pathological glucose tolerance or diabetes mellitus type II. Metabolic syndrome is diagnosed too seldom in view of the fact that a prevalence of at least 10% must be assumed for the population as a whole. Besides genetic predisposition, environmental factors such as diet, physical inactivity and nicotine and alcohol consumption play a decisive role in its clinical manifestation. The paper briefly examines the pathophysiological connections between the individual findings, with the central role of insulin resistance being emphasized. With a multifactorial therapy, in which non-medicamentous treatment is predominant, it must be assumed that on the whole compliance will tend to be poor. Prognostically the syndrome is serious, very frequently resulting in premature atherosclerosis. The paper concludes with a consideration of the underwriting of metabolic syndrome, one of the points being that the extramortality rates of the individual impairments should not be applied additively.
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PMID:[Prognostic aspects of metabolic syndrome. Is the "good living" syndrome regarded seriously enough in general insurance medicine practice?]. 901 97


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