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

Caloric restriction in animal models delays many age-related pathological conditions. Ageing rats have characteristically increased body weight, fat mass and a specific body fat distribution. This report will focus on the potential cause-effect relationship between increased fat mass and accelerated ageing. In humans, increased fat mass (obesity), and in particular increases in abdominal obesity as a result of deposition of visceral fat, are associated with the metabolic syndrome of ageing. This syndrome is associated with hyperinsulinaemia, dyslipidaemia, type 2 diabetes mellitus, atherosclerosis, hypercoagulability and hypertension. Fat tissue, however, plays a major role by secreting multiple metabolically active factors, which are potentially responsible for the development of insulin resistance. This article will review various experimental models (in animals) used to prevent insulin resistance of ageing by decreasing fat mass, and in particular, decreasing visceral fat. We suggest that this decrease in fat mass and its beneficial repercussions observed in ageing animal models may apply also to human ageing and its related pathology.
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PMID:Caloric restriction, body fat and ageing in experimental models. 1496 3

Abdominal obesity and insulin resistance are central findings in metabolic syndrome. Since treatment with recombinant human growth hormone (rhGH) can reduce body fat mass in patients with organic GH deficiency, rhGH therapy may also have favourable effects on patients with metabolic syndrome. However, due to the highly increased risk for type 2 diabetes in these patients, strategies are needed to reduce the antagonistic effect of rhGH against insulin. We conducted a 18-month randomised, double-blind, placebo-controlled study to assess the effect of rhGH in combination with metformin (Met) in patients with metabolic syndrome. 25 obese men (55 +/- 6 years, BMI 33.4 +/- 2.9 kg/m (2)) with mildly elevated fasting plasma glucose (FPG) levels at screening (6.1-8.0 mmol/l) were included. All patients received metformin (850 mg twice daily) either alone or in combination with rhGH (daily dose 9.5 microg/kg body weight). An oGTT was performed at baseline, after 6 weeks, and after 3, 6, 12, and 18 months of therapy. Glucose disposal rate (GDR) was measured by euglycemic hyperinsulinemic clamp at 0 and 18 months and body composition was measured by DEXA every 6 months. In the Met + GH group, IGF-I increased from 146 +/- 56 microg/l to 373 +/- 111 microg/l (mean +/- SD) after 3 months and remained stable after that. BMI did not change significantly in either group during the study. Total body fat decreased by -4.3 +/- 5.4 kg in the Met + GH group and by -2.7 +/- 2.9 kg in the Met + Placebo group (differences between the two groups: p = n. s.). Waist circumference decreased in both groups (Met + GH: 118 +/- 8 cm at baseline, 112 +/- 10 cm after 18 months; Met + Placebo: 114 +/- 7 cm vs. 109 +/- 8 cm; differences between the two groups: p = 0.096). In the Met + GH group, FPG increased significantly after 6 months (5.9 +/- 0.7 vs. 6.7 +/- 0.4 mmol/l; p = 0.005), but subsequently decreased to baseline levels (18 months: 5.8 +/- 0.2 mmol/l). FPG remained stable in the Met + Placebo group until 12 months had elapsed, and then slightly decreased (baseline: 6.2 +/- 0.3, 18 months: 5.5 +/- 0.6 mmol/l, p = 0.02). No significant changes were seen in either group regarding glucose and insulin AUC during oGTT or HbA (1c) levels. GDR at 18 months increased by 20 +/- 39% in Met + GH-group and decreased by -11 +/- 25% in the Met + Placebo group (differences between the two groups: p = 0.07). In conclusion, treatment of patients with metabolic syndrome and elevated FPG levels did not cause sustained negative effects on glucose metabolism or insulin sensitivity if given in combination with metformin. However, since our data did not show significant differences between the two treatment groups with respect to body composition or lipid metabolism, future studies including larger numbers of patients will have to clarify whether the positive effects of rhGH on cardiovascular risk factors that have been shown in patients with GH deficiency are also present in patients with metabolic syndrome, and are additive to the effects of metformin.
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PMID:Effects of a combination of recombinant human growth hormone with metformin on glucose metabolism and body composition in patients with metabolic syndrome. 1498 8

Obesity is a major risk factor for several metabolic diseases, frequently clustering to form the metabolic syndrome, carrying a high risk of cardiovascular mortality. We aimed to assess the prevalence of the metabolic syndrome in treatment-seeking obese subjects and the potential protective effect of physical activity. A cross-sectional analysis of data from a large Italian database of treatment-seeking obese subjects was performed. The metabolic syndrome was defined according to the criteria provisionally set by the National Cholesterol Education Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, based on waist circumference, fasting glucose, triglyceride (TG) and high-density lipoprotein-cholesterol (HDL-C) levels, and arterial pressure. Data were available in 1,889 Caucasian subjects, 78% females, from 25 obesity centers. Minimum criteria for the metabolic syndrome were fulfilled in 53% of cases. The prevalence increased with age and obesity class and was negatively associated with participation in a structured program of physical activity (odds ratio, 0.76; 0.58 to 0.99; P =.041), after correction for age, sex, and body mass. The prevalence of cardiovascular disease was higher in subjects with the metabolic syndrome. A subset of 12.8% of cases had no metabolic abnormalities. They had a lower prevalence of abdominal obesity and cardiovascular disease. Isolated obesity was significantly associated with physical activity (odds ratio, 1.86; 1.33 to 2.60; P =.0003). Multiple metabolic disorders are present in most obese patients, and their prevalence is lower in physically active subjects. It is time to move towards a more integrated approach and to reconsider resource allocation to improve lifestyle changes for large-scale control of obesity.
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PMID:The metabolic syndrome in treatment-seeking obese persons. 1504 88

The metabolic syndrome comprises a set of metabolic and physiologic risk factors associated with elevated cardiovascular disease risk. The expression of each one of its major factors (hypertriglyceridemia, low high-density lipoprotein cholesterol levels, hypertension, abdominal obesity, and insulin resistance) has been found to be the result of complex interactions between genetic and environmental factors. Moreover, obesity may play a major role in triggering the metabolic syndrome by interacting with genetic variants at candidate genes for dyslipidemia, hypertension, and insulin resistance. In support of this hypothesis, several studies at multiple candidate genes have already demonstrated the significance of these interactions; however, the data and their reliability are still very limited, and in many cases replication studies are still lacking in the literature. Therefore, more studies with better epidemiologic design and standardized adiposity measures are needed to estimate the contribution of body weight and fat distribution to the genetic predisposition to the metabolic syndrome, which is the most common cardiovascular disease risk factor in industrialized societies.
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PMID:The metabolic syndrome: a crossroad for genotype-phenotype associations in atherosclerosis. 1506 43

This study aimed to estimate nationwide prevalence of the metabolic syndrome and to identify its association with cardiovascular diseases. The data on a national representative sample of 6,147 adults from 1998 Korea National Health and Nutrition Survey were analyzed. The syndrome was determined according to two kinds of modified definition from ATP III, in which abdominal obesity was determined by waist circumference (WC) standard for Asians and waist-to-hip ratio (WHR). Based on the former, prevalence was 22.1% in men and 27.8% in women. However, based on the latter, prevalence was 28.6% and 27.8%, respectively. Although age-specific prevalence was higher in men than in women among the younger group, it became higher in women among the older group because of its steeper rise with age. In multiple logistic regression, the syndrome was found to be positively associated with cardiovascular diseases (adjusted odds ratios (ORs)1.97 by WC and 1.48 by WHR in men, and 1.54 and 1.31 in women). Moreover, its effect size exceeded that of total cholesterol (adjusted ORs 1.21 in men, and 1.08 in women) or LDL cholesterol (1.58 in men and 1.22 in women). It is obvious that the metabolic syndrome prevails in Korea, and its importance regarding cardiovascular diseases is considerable. Prevention strategies should be implemented immediately to avoid cardiovascular epidemic in the near future.
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PMID:Prevalence of the metabolic syndrome and its association with cardiovascular diseases in Korea. 1508 90

Metabolic syndrome is defined as a clustering of cardiovascular risk factors (abdominal obesity, hyperinsulinemia, atherogenic dyslipidemia, hypertension and hypercoagulability) that together increase the risk of developing coronary heart disease and type 2 diabetes. Inhibition of acetyl-CoA carboxylase (ACC), which results in inhibition of fatty acid synthesis and stimulation of fatty acid oxidation, has the potential to favorably affect a multitude of cardiovascular risk factors associated with metabolic syndrome. ACC exists as two tissue-specific isozymes, ACC1 present in lipogenic tissues (liver and adipose) and ACC2 present in oxidative tissues (liver, heart and skeletal muscle). Studies in both ACC2 knockout mice and animals administered isozyme-nonselective ACC inhibitors have demonstrated the utility of treating metabolic syndrome through this modality. An isozyme-non-selective ACC inhibitor may potentially provide the optimal therapeutic for beneficially affecting metabolic syndrome. However, demonstration of the full potential of isozyme-selective inhibitors, once identified, should reveal advantages and liabilities associated with single isozyme inhibition. While demonstrating clinical efficacy of an ACC inhibitor should be relatively straightforward, the heterogeneity of the patient population and the absence of established guidelines regarding approval endpoints for agents simultaneously affecting multiple aspects of metabolic syndrome will pose developmental challenges for initial market entries.
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PMID:Acetyl-CoA carboxylase inhibition for the treatment of metabolic syndrome. 1508 94

About 60% of patients with mild and moderate hypertension have insulin resistance and half of them have clinically manifest metabolic syndrome which comprises abdominal obesity, hyperlipidemia, impaired glucose tolerance, hypertension and insulin resistance. In a framework of metabolic syndrome hypertension is characterized by disturbed circadian profile without nocturnal blood pressure lowering and concentric left ventricular hypertrophy. There exist 2 mechanisms of linkage between hypertension and metabolic syndrome: impaired ion transport and neurohormonal and humoral activation. Antihypertensive drugs for correction of hypertension in metabolic syndrome should be long acting, provide protection of target organs, and induce positive or neutral metabolic effect. Together with normalization of blood pressure these actions can cause lowering of risk of atherosclerosis development. Representatives of the following classes of antihypertensive agents can be used as drugs of choice: angiotensin converting enzyme inhibitors, long-acting calcium antagonists, selective beta1-adrenoblockers, and thiazide diuretics.
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PMID:[Arterial hypertension in a framework of metabolic syndrome: special features and principles of drug correction]. 1511 79

Polycystic ovary syndrome (PCOS) is a heterogeneous clinical condition. In most women, especially in the obese, all features of the metabolic syndrome, particularly insulin resistance and associated hyperinsulinaemia, are present. Insulin is a physiological hormone regulating ovarian function, specifically ovarian steroidogenesis and androgen blood transport and/or activity in the target tissues. Hyperinsulinaemia may therefore play a pivotal role in favouring the hyperandrogenic state and related clinical and metabolic alterations. The abdominal obesity phenotype is common, affecting more than half of PCOS women. Menstrual cycles and fertility rate are negatively affected by the presence of insulin resistance, hyperinsulinaemia and obesity. PCOS women with obesity and insulin resistance are the obvious target for lifestyle intervention, such as changes in dietary habits and increased physical activity. Weight loss should therefore represent the first-line approach in the treatment of obese PCOS women, since it significantly improves hormonal and metabolic abnormalities and may favour spontaneous ovulation and improve fertility rate in the majority of patients. Individualized pharmacological support aimed at favouring weight loss and maintenance and improving insulin resistance may play a complementary role to lifestyle intervention.
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PMID:Role of changes in dietary habits in polycystic ovary syndrome. 1514 67

The metabolic syndrome is intended to identify patients who have increased risk of diabetes and/or a cardiac event due to the deleterious effects of weight gain, sedentary lifestyle, and/or an atherogenic diet. The National Cholesterol Education Program's Adult Treatment Panel III definition uses easily measured clinical findings of increased abdominal circumference, elevated triglycerides, low high-density lipoprotein-cholesterol, elevated fasting blood glucose and/or elevated blood pressure. Three of these five are required for diagnosis. The authors also note that other definitions of metabolic syndrome focus more on insulin resistance and its key role in this syndrome. This review focuses on how treatment might affect each of the five components. Abdominal obesity can be treated with a variety of lower calorie diets along with regular exercise. Indeed, all of the five components of the metabolic syndrome are improved by even modest amounts of weight loss achieved with diet and exercise. For those with impaired fasting glucose tolerance, there is good evidence that a high fiber, low saturated fat diet with increased daily exercise can reduce the incidence of diabetes by almost 60%. Of note, subjects who exercise the most, gain the most benefit. Metformin has also been shown to be helpful in these subjects. Thiazolidinedione drugs may prove useful, but further studies are needed. Although intensified therapeutic lifestyle change will help the abnormal lipid profile, some patients may require drug therapy. This review also discusses the use of statins, fibrates, and niacin. Likewise, while hypertension in the metabolic syndrome benefits from therapeutic lifestyle change, physicians should also consider angiotensin converting enzyme inhibitor drugs or angiotensin receptor blockers, due to their effects on preventing complications of diabetes, such as progression of diabetic nephropathy and due to their effects on regression of left ventricular hypertrophy. Aspirin should be considered in those with at least a 10% risk of a coronary event over 10 years. Finally, three related conditions, nonalcoholic fatty liver disease, polycystic ovary syndrome and protease inhibitor associated lipodystrophy improve with therapeutic lifestyle change. Although metformin is shown to be useful with polycystic ovary syndrome, the data supporting drug therapy for the other syndromes is less convincing. More robust studies are needed before any firm recommendations can be made.
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PMID:Treatment of metabolic syndrome. 1515 70

Alstrom syndrome (ALMS) is a very rare genetic autosomal recessive disease, characterized by early-onset severe abdominal obesity, impaired glucose tolerance or type 2 diabetes with insulin resistance, acanthosis nigricans, hyperlipidemia, childhood progressive retinal degeneration or retinitis pigmentosa and neurosensory hearing loss or deafness, cardiomyopathy, and other endocrine disorders. Genetic studies locate the ALMS gene on chromosome 2p12-13. The aim of this paper is to describe and discuss two unrelated cases of a mild ALMS form diagnosed after the age of 40 and 60, respectively, in adult fertile female patients. These cases showed several features of the disease plus other alterations characteristic of the classic "metabolic syndrome," including hypertension, hyperfibrinogenemia, and thrombotic states. Moreover, the patients had very high fasting serum free fatty acid (FFA) levels (2150 and 1919 micromol/L, respectively), which proved to be sensitive to inhibition by oral glucose tolerance test (OGTT)-induced hyperinsulinemia as well as to caloric restriction. ALMS may have an adverse prognosis and is often underdiagnosed. Its mild form, which allows a long survival, may also be associated with the late complications of the metabolic syndrome, leading to increased vascular risk.
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PMID:A mild form of Alstrom disease associated with metabolic syndrome and very high fasting serum free fatty acids: two cases diagnosed in adult age. 1516 53


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