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

With increasing numbers of cancer survivors, attention has been drawn to long-term complications of curative cancer treatment, including a range of metabolic disorders. These metabolic disorders often resemble the components of the so-called metabolic syndrome, or syndrome X, which is an important risk factor for the development of cardiovascular disease. The mechanisms behind the development of metabolic disorders in cancer survivors have not been fully elucidated. However, association studies in the general population have demonstrated correlations between the components of the metabolic syndrome on the one hand and hormonal deficiencies, hypomagnesaemia, and endothelial dysfunction on the other. These latter disorders are regularly reported following curative cancer treatment and could, therefore, be important aetiologic factors in the development of the metabolic syndrome in cancer survivors. This review discusses data on the associations between the metabolic syndrome and treatment-related complications in cancer survivors and possibilities for preventive measures.
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PMID:The metabolic syndrome in long-term cancer survivors, an important target for secondary preventive measures. 1236 60

The three major components of dyslipidemia associated with the metabolic syndrome are increased fasting and postprandial triglyceride-rich lipoproteins (TRLs), decreased high-density lipoprotein (HDL), and increased small, dense low-density lipoprotein (LDL) particles. Insulin resistance and compensatory hyperinsulinemia lead to overproduction of very low-density lipoprotein particles. A relative deficiency of lipoprotein lipase, an insulin-sensitive enzyme, is partly responsible for the decreased clearance of fasting and postprandial TRLs, and the decreased production of HDL particles. The resulting increased concentration of cholesteryl ester-rich fasting and postprandial TRLs is the central lipoprotein abnormality of the metabolic syndrome. The increase of small, dense LDL particles, and decrease of large, buoyant HDL particles are consequential events. All these lipoprotein defects contribute largely to the increased cardiovascular disease risk in individuals with insulin resistance. Peroxisome proliferator-activated receptor (PPAR)a, PPARg, and PPARd agonists seem to improve dyslipidemia of the metabolic syndrome by regulating the expression of important genes involved in the deranged lipoprotein metabolism associated with insulin resistance.
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PMID:Dyslipidemia of the metabolic syndrome. 1237 72

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.
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PMID:The foetal origins of the metabolic syndrome--a South African perspective. 1238 59

In westernised societies the metabolic syndrome (MS) is common and primarily a lifestyle disease with significant morbidity and premature mortality. The main endpoints are related to cardiovascular disease (CVD), especially affecting the heart. Although insulin resistance (and hyperinsulinaemia) is an early marker of MS and future adverse cardiovascular outcomes, it is not known if on its own this is sufficient. The issue is further clouded in prospective studies by the development in study subjects of some, or all of the components of MS, each of which is an independent risk factor for CVD! Therefore, in spite of a number of appropriate long-term observational studies, we are unable to tease out the exact contribution of the individual components of MS, which together are unequivocally responsible for this present-day epidemic of CVD.
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PMID:The metabolic syndrome, insulin resistance and cardiovascular disease. 1238 61

Abnormalities in fatty acid (FA) metabolism underlie the development of insulin resistance and alterations in glucose metabolism, features characteristic of the metabolic syndrome and type 2 diabetes that can result in an increased risk of cardiovascular disease. We present pharmacodynamic effects of AZ 242, a novel peroxisome proliferator activated receptor (PPAR)alpha/gamma agonist. AZ 242 dose-dependently reduced the hypertriglyceridemia, hyperinsulinemia, and hyperglycemia of ob/ob diabetic mice. Euglycemic hyperinsulinemic clamp studies showed that treatment with AZ 242 (1 micromol/kg/d) restored insulin sensitivity of obese Zucker rats and decreased insulin secretion. In vitro, in reporter gene assays, AZ 242 activated human PPARalpha and PPARgamma with EC(50) in the micro molar range. It also induced differentiation in 3T3-L1 cells, an established PPARgamma effect, and caused up-regulation of liver fatty acid binding protein in HepG-2 cells, a PPARalpha-mediated effect. PPARalpha-mediated effects of AZ 242 in vivo were documented by induction of hepatic cytochrome P 450-4A in mice. The results indicate that the dual PPARalpha/gamma agonism of AZ 242 reduces insulin resistance and has beneficial effects on FA and glucose metabolism. This effect profile could provide a suitable therapeutic approach to the treatment of type 2 diabetes, metabolic syndrome, and associated vascular risk factors.
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PMID:AZ 242, a novel PPARalpha/gamma agonist with beneficial effects on insulin resistance and carbohydrate and lipid metabolism in ob/ob mice and obese Zucker rats. 1240 84

Gender-specific differences in the incidence of cardiovascular disease have long been known, and estrogens have been considered to be responsible for this dissimilarity. Recently, the steep increase in cardiovascular risk in the no longer fertile woman has become evident. The postmenopausal metabolic syndrome is very frequent, with obesity, insulin resistance, and hyperinsulinemia, which convey increased sodium reabsorption, stimulation of the sympathetic nervous system, and smooth muscle growth. The clinical corollary of these overall changes is hypertension. Gender differences in components of the renin-angiotensin system have been shown to exist, and may play a central role in blood pressure control. In normotensive populations, plasma renin activity is significantly higher in men than in women, and is higher in postmenopausal versus premenopausal women. Two angiotensin-converting enzyme inhibitors, ramipril and moexipril, have undergone trials aimed specifically at older people with cardiovascular risk and with postmenopausal hypertension, and could be the first therapeutic choice. However, a comprehensive treatment should include nonpharmacologic measures with strong emphasis on weight normalization and regular physical activity, prevention of osteoporosis, as well as decisions on the use of estrogen replacement therapy and treatment of the menopausal metabolic syndrome. Finally, education of both patients and physicians on the nature and prognosis of untreated hypertension is crucial.
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PMID:Systemic hypertension in postmenopausal women: a clinical approach. 1241 76

Obesity is a recognized risk factor for cardiovascular disease. Because the prevalence of obesity is rising in industrialized as well as developing nations, it is important to understand the mechanisms by which obesity targets the vascular system. A metabolic syndrome of insulin resistance is provoked by obesity, and this results in the dysregulation of a number of adipocyte-derived factors, which favors atherosclerosis. This review focuses on how products of the adipocyte, including free fatty acids and "adipo"-cytokines, may mediate the effect of obesity on insulin resistance and atherosclerosis.
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PMID:Molecular links between obesity and cardiovascular disease. 1242 10

This invesgation examined the impact of hostility and the metabolic syndrome on coronary heart disease (CHD) using prospective data from the Normative Aging Study. Seven hundred seventy-four older, unmedicated men free of cardiovascular disease were included in the study. The total Cook-Medley Hostility (Ho) Scale score, anthropometric data, serum lipids, fasting insulin concentrations, blood pressure, cigarette smoking, alcohol consumption, and total dietary calories were used to predict incident CHD during a 3-year follow-up interval. Multivariate analysis indicated that only Ho positively predicted and high-density lipoprotein cholesterol level negatively predicted incident CHD. Ho's effects on CHD may be mediated though mechanisms other than factors that constitute the metabolic syndrome.
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PMID:Hostility, the metabolic syndrome, and incident coronary heart disease. 1243 11

The most common and clinically important complication in adults with diabetes is cardiovascular disease (CVD), which includes coronary heart disease, peripheral vascular disease, and stroke. Both type 2 diabetes and the insulin resistance syndrome are associated with a marked increase in the risk for CVD. The metabolic syndrome and the closely related insulin resistance syndrome have recently been recognized as important disorders, each being associated with an increase in CVD risk even in the absence of glucose intolerance. Given the significant public health burden of CVD, risk reduction has emerged as a significant clinical challenge for most practitioners. Diabetes and the insulin resistance syndrome are closely related disorders, with insulin resistance being more than a key pathogenic defect in type 2 diabetes. Even in the absence of glucose intolerance, these 2 disorders are both associated with a number of distinct pathologic findings, including hypertension, atherogenic dyslipidemia, a prothrombotic environment, and significant vascular and hemodynamic abnormalities that result from endothelial cell dysfunction. Insulin resistance is now recognized to be closely associated with the development of each of these risk factors. This article uses a case-based approach to discuss the unique features of insulin resistance and type 2 diabetes considered to be key contributors to CVD risk. A systematic approach to both evaluation and management is proposed, with priority given to therapies of demonstrated clinical benefit. Because of its critical and central role in the development of many CVD risk factors, targeted treatment of insulin resistance will also be discussed as such therapy may prove to be a critical component of care in years to come.
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PMID:The metabolic syndrome, type 2 diabetes, and cardiovascular disease: understanding the role of insulin resistance. 1251 Jul 88

Nutritional interventions may favourably regulate dyslipoproteinemia and, hence, decrease cardiovascular disease risk. Lipoprotein kinetic studies afford a powerful approach to understanding and defining the mechanisms by which such interventions modulate lipoprotein metabolism. Stable isotope tracers and compartment models are now commonly employed for such studies. We review the recent application of tracer methodologies to the study of dyslipoproteinemia in the metabolic syndrome. We also focus on the effects of nutritional intervention studies that have addressed the effects of weight loss, n-3 fatty acids, plant sterols and alcohol on very low density lipoprotein, LDL and HDL metabolism. The potential for statin treatment as an adjunct to dietary modification is also discussed. New tracer methodologies are discussed, specifically those referring to reverse cholesterol transport. The nutritional interventions discussed in this review are readily transferable into clinical preventive practice. The potential benefits to be gained by weight loss and fish oil supplementation in the metabolic syndrome extend beyond their specific and positive effects on lipoprotein metabolism. Furthermore, recent developments in tracer methodologies afford new tools for probing the in-vivo pathways of lipoprotein metabolism in future studies.
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PMID:Kinetic studies of lipoprotein metabolism in the metabolic syndrome including effects of nutritional interventions. 1254 63


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