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

Recent studies have indicated that the waist/hip circumference ratio (WHR), an index of abdominal fat distribution, is a risk factor for cardiovascular disease and diabetes, in parallel with other previously established risk factors. Obesity, without taking fat distribution into account, seems to be associated with WHR in its relationship to the metabolic risk factors for these diseases. The important component of the WHR is probably the mass of visceral fat. This cluster of phenomena constitute what has recently been called the metabolic syndrome or syndrome X. Visceral fat mass is probably increased by a multiple endocrine aberration, where steroid hormones are important. This seems to cause insulin resistance by direct effects on the periphery, which may be amplified by the metabolism of the enlarged visceral adipose tissues.
J Cardiovasc Pharmacol 1992
PMID:Abdominal fat distribution and the metabolic syndrome. 128 66

The study was undertaken to evaluate the development and association of parameters related to the metabolic syndrome during celiprolol treatment. Hyperinsulinemic euglycemic clamp and independent oral glucose tolerance tests (OGTT) were performed on 25 nondiabetic patients with controlled hypertension and dyslipidemia. The tests were carried out during the patients' previous antihypertensive monotherapy (beta- or Ca-blocker, or an ACE inhibitor), and after 6 and 12 months of celiprolol treatment. About one third of patients were randomized to a control group in which treatment was kept unchanged. Insulin sensitivity index (ISI), measured by the euglycemic clamp test, increased 35% in the celiprolol group at 6 months and remained at that level at 12 months, independent of the previous treatment (p = 0.03, compared to the change in the control group). During a 2 hour OGTT, incremental glucose area under the curve (AUC) decreased from 4.5 to 1.9 hr x mmol/l during 6 months of celiprolol treatment, and decreased further to 1.5 hr x mmol/l at 12 months (p < 0.001). Insulin AUC decreased from 113 to 72 hr x mU/l, and decreased further to 68 hr x mU/l (p < 0.01). All insulin parameters in OGTT were highly significant (p < 0.0001) and inversely associated with ISI. Insulin AUC had the best linear correlation with ISI (r = -0.682, p < 0.0001). Glucose parameters in OGTT correlated only weakly and inversely with insulin sensitivity. From the fasting serum lipids, triglycerides showed an inverse (p < 0.001) and HDL a weak (p < 0.05) positive association with ISI. Four out of 20 metabolic, clinical, and demographic parameters proved to be independently significant predictors for ISI in multiple regression analysis. These were insulin AUC, fasting insulin levels, triglyceride values, and age. The coefficient of determination in this four-parameter linear model was 69%. In this preliminary, observer-masked trial with a limited control group, celiprolol improved the impaired insulin sensitivity and glucose tolerance of dyslipidemic hypertensive patients. A fairly predictive model can be formulated to evaluate the peripheral insulin sensitivity of hypertensive patients with suspected metabolic syndrome using OGTT with serum insulin determinations.
Cardiovasc Drugs Ther 1995 Apr
PMID:Association between serum lipids, glucose tolerance, and insulin sensitivity during 12 months of celiprolol treatment. 766 96

A 67-year-old man was admitted with traumatic arterial occlusion in his leg 24 h after an accident. A double-lumen catheter was inserted into the left iliac vein, after revascularization, and haemodialysis started using a new membrane dialyser to remove myoglobin effectively. Intramuscular pressure of the limb was measured and, when it was 35 mmHg, staged fasciotomy was performed. A modification of the procedure used to prevent myonephropathic metabolic syndrome and compartment syndrome is described.
Cardiovasc Surg 1994 Aug
PMID:Immediate haemodialysis and staged fasciotomy in the treatment of reperfusion injury. 795 61

The reduction of coronary mortality is not as large as one would expect from the observed blood pressure lowering in trials of antihypertensive medications. This is not surprising; hypertension is a complex disease where the high blood pressure is only one of numerous coronary risk factors. Sympathetic overactivity in hypertension, independent of the blood pressure, may be conducive to premature atherosclerosis by inducing insulin resistance and dyslipidemia. Through its trophic effect on blood vessels, sympathetic overactivity potentiates vasoconstriction. This, in turn, accelerates hypertension and the metabolic syndrome. The hypertrophy of small coronary arterioles decreases the coronary reserve and enhances coronary spasms. Tachycardia, which is due to increased sympathetic tone and a decreased parasympathetic tone, favors arrhythmias and sudden death in congestive heart failure and hypertension. Increased hematocrit is frequently found in male patients with hypertension, and high hematocrit is a predictor of coronary heart disease/thrombosis. The increase of hematocrit is in part due to an alpha adrenergic postcapillary venoconstriction. Enhanced sympathetic drive, insulin resistance and dyslipidemia have been demonstrated also in congestive heart failure, but the clinical importance of these findings is not fully understood.
Scand Cardiovasc J Suppl 1998
PMID:Clinical consequences of the autonomic imbalance in hypertension and congestive heart failure. 954 Jan 30

The JCR:LA-cp rat is a unique strain that, if homozygous for the autosomal recessive cp gene, is obese and exhibits the metabolic syndrome of insulin resistance, hyperinsulinemia, and hypertriglyceridemia. Obese male rats spontaneously develop advanced atherosclerosis and ischemic myocardial lesions. The angiotensin-converting enzyme inhibitor, captopril, was administered to obese rats at 30 mg/kg body weight from 6 to 39 weeks of age. There were no significant changes in food consumption or body weights of the treated animals. Insulin sensitivity was not improved. Plasma insulin levels were unaltered, but the volume density of the islets of Langerhans was halved, reflecting both reduced hyperplasia and a more normal islet structure. Triglyceride concentrations were not reduced, but unesterified cholesterol and cholesteryl esters decreased by 50% and 34%, respectively (p < 0.01). The impaired nitric oxide-mediated vascular relaxation of the obese rats was not improved, and the relaxant sensitivity to acetylcholine as indicated by the median effective concentration (EC50) was reduced. In vitro, captopril significantly reduced the basal tension of aortic rings from untreated rats, antagonized the contractile effects of norepinephrine, and induced complete relaxation of the contraction in response to 10(-7) M norepinephrine. The severity of spontaneous, raised atherosclerotic lesions of the aortic arch at age 39 weeks was not significantly decreased by captopril treatment. In contrast, the frequency of ischemic myocardial lesions was reduced by 78% (p < 0.01). The protective effects of captopril on the heart and pancreas in this animal model of type II diabetes and atherosclerosis are probably the result of its bradykinin-enhancing effects.
J Cardiovasc Pharmacol 1998 Jun
PMID:Inhibition of myocardial lesions in the JCR:LA-corpulent rat by captopril. 964 85

We examined the effects of the potassium channel opener KRN4884 (5-amino-N-[2-(2-chlorophenyl)ethyl]-N'-cyano-3-pyridinecarboxamidine ) on cardiovascular metabolic syndrome (i.e., syndrome X), in rats. High-fructose diet rats developed hypertension, hypertriglyceridemia, increased total cholesterol/HDL (high-density lipoprotein)-cholesterol ratio, and hyperinsulinemia, KRN4884 (0.3-3.0 mg/kg, twice a day for 14 days, p.o.) alleviated the risk factors in fructose-fed rats. Furthermore, fructose-fed rats exhibited impairment of glucose tolerance and excess insulin secretion when loaded with glucose orally. Treatment with KRN4884 (1.0 mg/kg, twice a day for 14 days, p.o.) improved the glucose intolerance and inhibited hypersecretion of insulin in the glucose-loaded, fructose-fed rats. In contrast, KRN4884 (0.3-1.0 mg/kg, twice a day for 10 days, p.o.) did not affect serum triglyceride, cholesterol, glucose, or insulin concentrations in normal rats. LPL (lipoprotein lipase) activities in skeletal muscle and adipose tissue, and HTGL (hepatic triglyceride lipase) activity in liver were measured after administration of KRN4884 or vehicle twice a day for 14 days in fructose-fed rats. KRN4884 caused a significant increase in LPL activity in muscle and tended to increase LPL activity in adipose tissue in fructose-fed rats. HTGL was decreased in fructose-fed rats as compared with normal controls and was unaffected by KRN4884. These findings suggested that KRN4884 enhances insulin sensitivity and LPL activity, which are related to glucose and lipid metabolism and may be useful for the treatment of syndrome X.
J Cardiovasc Pharmacol 2000 Feb
PMID:Effects of the K+ channel opener KRN4884 on the cardiovascular metabolic syndrome model in rats. 1067 63

In recent years, interest has tended to focus on prevention of coronary events in high-risk groups, particularly those with established coronary heart disease. While this is understandable, it has led to a lack of emphasis on primary prevention. Yet it is only by means of primary or even pri-mordial prevention that a substantial reduction in coronary mortality on a population level will be achieved. This becomes clear when we consider that half of all persons who suffer a first myocardial infarction will die within the first month thereafter. Nevertheless, major progress has been made in primary prevention. Reliable risk algorithms have been constructed in Europe (PROCAM) and the U.S., and preliminary analyses on both sides of the Atlantic indicate that these algorithms can be useful applied to populations which are geographically and ethnically distinct from those in which they were derived. A notable trend in recent years is the increasing recognition of the metabolic syndrome with its key components of abdominal obesity, hypertriglyceridemia hypertension, low HDL-C, small, dense LDL, insulin resistance and hyperinsulinemia as being perhaps the most common and dangerous metabolic abnormality of all. Newer risk markers are being evaluated. The position of homocysteine remains unclear. Despite a strong association of elevated homocysteine with risk in case-control studies, prospective investigations have been less convincing. Evidence is beginning to accumulate from cross-sectional and prospective studies that markers of inflammation such as C-reactive peptide may improve our ability to predict risk of coronary events. While these data are encouraging, results of further studies must be awaited before the true place of these markers can be determined. The same can be said of many genetic markers of risk. Though a very large number of association studies have indicated links between a variety of genetic markers and coronary risk, these effects have tended to disappear after controlling for epigenetic and confounding factors and with increasing sample sizes. Finally, much attention is being devoted to non-invasive imaging of the coronary arteries. Such methods hold much promise as a screening test to exclude coronary stenosis in low-risk individuals. However, the measurement of calcium content of the arterial wall by EBCT has yet to prove its usefulness as a predictor of coronary events.
Nutr Metab Cardiovasc Dis 2000 Jun
PMID:Primary prevention of coronary heart disease: from controversy to consensus. 1100 23

This paper reviews the clinical trial data that offer insight into the question of whether, and in what groups of people, triglycerides might be an appropriate therapeutic target for the primary or secondary prevention of atherosclerotic cardiovascular disease. Two angiographic trials (the Lopid Coronary Angiography Trial and the Bezafibrate Coronary Atherosclerosis Intervention Trial) and three clinical endpoint trials (the Helsinki Heart Study, the Bezafibrate Infarction Prevention Study, and the VA HDL Intervention Trial) are reviewed. Hypertriglyceridemia per se is probably not an appropriate therapeutic target for the prevention of atherosclerotic cardiovascular disease because it is a poor marker of atherogenic risk and because there have been no clinical trials that have directly addressed the question of whether lowering the triglyceride level reduces the number of clinical events. The studies reviewed here, however, suggest that patients with established coronary heart disease and a high triglyceride level, in association with either a low high-density lipoprotein-cholesterol level or perhaps other features of the metabolic syndrome, such as obesity, diabetes, or hypertension, may benefit from fibrate therapy. For patients without established coronary heart disease, it is reasonable to consider hypertriglyceridemia as a risk marker prompting the aggressive treatment of other risk factors such as hypertension, diabetes, high low-density lipoprotein-cholesterol, and obesity.
J Cardiovasc Risk 2000 Oct
PMID:Triglycerides and coronary heart disease: implications of recent clinical trials. 1114 64

A large body of experimental and epidemiological evidence has established an association between visceral obesity and the metabolic syndrome, which retains its power throughout the spectrum of adiposity and is still clinically meaningful in severe obesity. The association may be due to an overload of liver free fatty acids (FFA) produced by the high lipolytic activity of omental fat. A substantial improvement in all aspects of the metabolic syndrome with only a moderate degree of weight loss has been observed in a large number of randomised controlled studies and can also be obtained in severe obesity, despite the fact that the patients remain obese. The reasons for this apparent dissociation between weight loss and metabolic improvement are not yet clearly understood, but may involve the relationship between visceral fat and metabolic alterations. The results of some studies suggest that the favourable metabolic changes observed in obese patients with weight loss may be directly attributable to a reduction in visceral fat, and other studies have recently shown that a rapid and preferential reduction in visceral fat mass occurs during the first phase of weight loss in morbidly obese patients possibly as a result of sympathetic nervous system activation. It is therefore possible that the apparent dissociation between weight loss and metabolic improvement is partially due to a difference in the responsiveness of visceral and subcutaneous adipose tissue to energy restriction: i.e. the fact that the metabolic profile of patients with visceral obesity may substantially improve after the loss of only a few kilograms of body weight could be related to a greater relative reduction in the amount of visceral rather than other fat. In this respect, the characteristically high rate of visceral fat mobilisation can also be seen as a good target for interventions aimed at reducing cardiovascular risk factors.
Nutr Metab Cardiovasc Dis 2001 Jun
PMID:Visceral obesity and the metabolic syndrome: effects of weight loss. 1159 Sep 96

The developing world is experiencing a rise in the prevalence of obesity, diabetes and cardiovascular disease to such an extent that it is often described as an epidemic. The most common explanation advanced for this phenomenon is the so-called epidemiological transition, with the biological basis of the thrifty genotype. The thrifty genotype theory suggests that genes derived from times of deprivation may result in adaptations that have adverse effects in times of plenty. However, a divergent theory is the so-called foetal origins of chronic disease, which ascribes the epidemic, in part, to an adverse intrauterine environment. There is compelling evidence, based on large numbers of epidemiological studies conducted in both developing and developed countries, that small size at birth in full-term pregnancies is linked with the subsequent development of the major features of the metabolic syndrome, namely glucose intolerance, increased blood pressure, dyslipidaemia and increased mortality from cardiovascular disease.
Cardiovasc J S Afr
PMID:The foetal origins of the metabolic syndrome--a South African perspective. 1238 59


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