UMLS:C0311277 - FACTA Search

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Query: UMLS:C0311277 (abdominal obesity)
2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The regional distribution of body fat has been identified as a significant risk factor for the development of noninsulin-dependent diabetes mellitus and cardiovascular disease (CVD). Several studies that have investigated the potential associations between topographic features of adipose tissue and indices reflecting carbohydrate and lipid metabolism have reported significant associations between abdominal fat deposition and metabolic complications. The development of computed tomography as a means to precisely measure the amount of subcutaneous and deep adipose tissue at any site of the body has shown that determination of the level of visceral adipose tissue is a critical measurement to perform in the assessment of the health hazards of obesity. Studies that we have conducted in premenopausal women have clearly shown that the level of visceral adipose tissue is the best correlate of lipoprotein ratios used to estimate the risk of CVD. We have also reported that a high level of visceral adipose tissue is associated with a deterioration of glucose tolerance and that the relationship between visceral fat deposition and glucose tolerance remains significant after controlling for the level of total-body fat. Because significant interrelationships were observed between abdominal visceral obesity, insulin resistance, and dyslipoproteinemias in obese women, it is suggested that visceral obesity is an important component of the insulin-resistance syndrome (syndrome X) that has been previously described. This cluster of morphological, hormonal, and metabolic alterations observed in abdominal obesity may have substantial implications for the treatment of this condition.
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PMID:Abdominal obesity as important component of insulin-resistance syndrome. 828 86

Coronary heart disease, hypertension, non-insulin-dependent diabetes and obesity are major causes of ill health in industrial societies. Disturbances of carbohydrate and lipid metabolism are a common feature of these disorders. The bases for these disturbances and their roles in disease pathogenesis are poorly understood. The spontaneously hypertensive rat (SHR), a widely used animal model of essential hypertension, has a global defect in insulin action on glucose metabolism and shows reduced catecholamine action on lipolysis in fat cells. In our study we used cellular defects in carbohydrate and lipid metabolism to dissect the genetics of defective insulin and catecholamine action in the SHR strain. In a genome screen for loci linked to insulin and catecholamine action, we identified two quantitative trait loci (QTLs) for defective insulin action, on chromosome 4 and 12. We found that the major (and perhaps only) genetic determinant of defective control of lipolysis in SHR maps to the same region of chromosome 4. These linkage results were ascertained in at least two independent crosses. As the SHR strain manifests many of the defining features of human metabolic Syndrome X, in which hypertension associates with insulin resistance, dyslipidaemia and abdominal obesity, the identification of genes for defective insulin and catecholamine action in SHR may facilitate gene identification in this syndrome and in related human conditions, such as type-2 diabetes and familial combined hyperlipidaemia.
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PMID:Quantitative trait loci for cellular defects in glucose and fatty acid metabolism in hypertensive rats. 917 35

Obesity poses a serious health hazard and its treatment is often disappointing. Major advances have been made during recent years in the understanding of body weight regulation, with the discovery of leptin, a protein produced by adipocytes and acting on the central nervous system to reduce food intake, and that of beta-3 adrenergic receptors and uncoupling proteins which contribute to stimulate energy expenditure. Numerous metabolic complications are associated with abdominal obesity and most of them, such as diabetes mellitus, dyslipidaemias and arterial hypertension, appear to be linked to insulin resistance and may be part of the socalled metabolic syndrome or syndrome X. While very-low-calorie diets are usually effective in the short-term, they cannot, in the long-term and for most patients, solve the problem of severe obesity. Pharmacological antiobesity treatment may include drugs that reduce food intake, drugs that increase energy expenditure and drugs that affect nutrient partitioning or metabolism. All of these pharmacological approaches have potential efficacy, but unfortunately serious limitations. This is also the case of mechanical means, such as intragastric balloons. Consequently, bariatric surgery may be considered as a valuable alternative therapy in well-selected patients with morbid obesity refractory to classical treatments. In conclusion, obesity is a chronic disease and should be treated as such with reasonable expectations.
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PMID:Medical aspects of obesity. 1042 50

The association of several risk factors, obesity, dyslipoproteinemia, hepatic steatosis, insulin resistance and hypertension with Type 2 (non-insulin-dependent) diabetes mellitus and myocardial infarction has long been known and has been termed the "metabolic syndrome". In 1988 Reaven introduced syndrome X as the link between insulin resistance and hypertension. It has been suggested that a critical factor in the association between obesity, Type 2 diabetes and cardiovascular morbidity is the mass of intraabdominal fat. Striking similarities exist between the metabolic syndrome and untreated growth hormone (GH) deficiency in adults. The central findings in both these syndromes are abdominal/visceral obesity and insulin resistance. Other features common to both conditions are premature atherosclerosis and increased mortality from cardiovascular diseases. These similarities indicate that undetectable and low levels of GH may be of importance in the metabolic aberrations observed in both these conditions. Recent investigations have found that abdominal/visceral distribution of adipose tissue is associated with endocrine disturbances including increased activity of the hypothalamic-pituitary-adrenal axis and a blunted secretion of GH and sex steroids. Theoretically, these endocrine perturbations can be a consequence of obesity, but the endocrine aberrations may have causal effects. We studied moderately obese, middle-aged men with a preponderance of abdominal body fat. As a group, they had slight to moderate metabolic changes known to be associated with abdominal/visceral obesity. Nine months of GH treatment reduced their total body fat and resulted in a specific and a marked decrease in both abdominal subcutaneous and visceral adipose tissue. Moreover, insulin sensitivity improved and serum concentrations of total cholesterol and triglyceride decreased. Diastolic blood pressure also decreased. The finding that GH replacement in men with abdominal obesity can diminish the negative metabolic consequences of visceral obesity suggests that low levels of this hormone are of importance for the metabolic aberrations associated with visceral/abdominal obesity.
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PMID:Growth hormone and the metabolic syndrome. 1044 70

There is now much interest in the mechanisms by which altered lipid metabolism might contribute to insulin resistance as is found in Syndrome X or in Type II diabetes. This review considers recent evidence obtained in animal models and its relevance to humans, and also likely mechanisms and strategies for the onset and amelioration of insulin resistance. A key tissue for development of insulin resistance is skeletal muscle. Animal models of Syndrome X (eg high fat fed rat) exhibit excess accumulation of muscle triglyceride coincident with development of insulin resistance. This seems to also occur in humans and several studies demonstrate increased muscle triglyceride content in insulin resistant states. Recently magnetic resonance spectroscopy has been used to demonstrate that at least some of the lipid accumulation is inside the muscle cell (myocyte). Factors leading to this accumulation are not clear, but it could derive from elevated circulating free fatty acids, basal or postprandial triglycerides, or reduced muscle fatty acid oxidation. Supporting a link with adipose tissue metabolism, there appears to be a close association of muscle and whole body insulin resistance with the degree of abdominal obesity. While causal relationships are still to be clearly established, there are now quite plausible mechanistic links between muscle lipid accumulation and insulin resistance, which go beyond the classic Randle glucose-fatty acid cycle. In animal models, dietary changes or prior exercise which reduce muscle lipid accumulation also improve insulin sensitivity. It is likely that cytosolic accumulation of the active form of lipid in muscle, the long chain fatty acyl CoAs, is involved, leading to altered insulin signalling or enzyme activities (eg glycogen synthase) either directly or via chronic activation of mediators such as protein kinase C. Unless there is significant weight loss, short or medium term dietary manipulation does not alter insulin sensitivity as much in humans as in rodent models, and there is considerable interest in pharmacological intervention. Studies using PPARgamma receptor agonists, the thiazolidinediones, have supported the principle that reduced muscle lipid accumulation is associated with increased insulin sensitivity. Other potent systemic lipid-lowering agents such as PPARalpha receptor agonists (eg fibrates) or antilipolytic agents (eg nicotinic acid analogues) might improve insulin sensitivity but further work is needed, particularly to clarify implications for muscle metabolism. In conclusion, evidence is growing that excess muscle and liver lipid accumulation causes or exacerbates insulin resistance in Syndrome X and in Type II diabetes; development of strategies to prevent this seem very worthwhile.
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PMID:Triglycerides, fatty acids and insulin resistance--hyperinsulinemia. 1145 39

The term metabolic syndrome is used for describing a cluster of cardiovascular risk factors comprising abdominal obesity, glucose intolerance/type 2 diabetes mellitus, dyslipidaemia and hypertension. A concomitant presentation of all components of the syndrome is rare, therefore, in the view of most experts three out of the four main components are sufficient for defining the syndrome. Another recently identified component of high clinical significance is the impairment of the fibrinolytic system which is now frequently mentioned in extended definitions. This clustering of metabolic risk factors has been described in various combinations and given different names including insulin resistance syndrome or syndrome X. Unfortunately, there is no generally accepted definition so far. The original mentioning of the syndrome goes back to the late sixties, when the metabolic syndrome was described as a 'disorder of genetic adaptation becoming manifest following unrestricted food intake and/or muscular inacitvity'. In its modern meaning this term was propagated by Hanefeld and Leonhardt and by Kaplan, who also called the syndrome the 'deadly quartet' to emphasize its high atherogenic potential.
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PMID:Insulin resistance and the metabolic syndrome-a challenge of the new millennium. 1196 19

The Metabolic Syndrome, also known as Syndrome X, refers to a constellation of atherosclerotic risk factors, including insulin resistance, hyperinsulinemia, dyslipidemia, essential hypertension, and abdominal obesity. We review four major published studies involving animals and humans that may be linked together in a unified hypothesis and justify a comprehensive approach in the treatment of this ever-increasing syndrome.
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PMID:The Metabolic Syndrome: where are we and where do we go? 1239 50

Metabolic syndrome is a complex disorder and an emerging clinical challenge. It is considered a "multiplex" cardiovascular risk factor, in that each component of the cluster of abnormalities is a risk factor in its own right. Introduced as Syndrome X by Reaven in 1988 and also termed insulin resistance syndrome, metabolic syndrome is recognized clinically by the findings of abdominal obesity, elevated triglycerides, atherogenic dyslipidemia - i.e. low levels of high-density lipoprotein cholesterol (HDL-C), elevated blood pressure, high blood glucose and/or insulin resistance. The goal of our research was to investigate intensity of "complete metabolic syndrome"- (abdominal obesity, dyslipidemia, elevated blood pressure, high blood glucose and/or insulin resistance) in patients with different degrees of obesity. In our study 570 patients have been involved. The patients were divided into 3 groups: I group--123 patients with first degree of obesity (body mass index - BMI - 30-34,9 kg/m2), II group--189 patients with II degree of obesity (BMI - 35-39,9 kg/m2), III group--258 patients with III degree of obesity (BMI >40 kg/m2). Results of carried out investigations have shown that the complete picture of metabolic syndrome was present in 132 (23,16%) patients and should note, that according to the increasing of obesity degrees also increases the intensity of metabolic syndrome.
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PMID:[Intensity of metabolic syndrome in patients with different degrees of obesity]. 1690 22

Although first knowledge on the joint onset of cardiovascular risk factors had been gained earlier, the first systematic review of this condition was made by G. Reaven in 1988 with his thesis on syndrome X, today known as the metabolic syndrome, with insulin resistance as the common denominator. Four elements have been identified: central obesity, dyslipoproteinemia (increased triglycerides, reduced HDL cholesterol), hypertension and glucose intolerance. There are two most influential definitions: one by the National Cholesterol Education Program (NCEP) and the other by the International Diabetes Federation (/IDF). NCEP requires the presence of at least three of the following factors: abdominal obesity as assessed by waist circumference >102 cm (m) or >88 cm (f), dyslipoproteinemia defined as triglyceridemia > or =1.7 mmol/L and/or HDL cholesterol <1.03 mmol/L (m); <1.29 mmol/L (f), hypertension (blood pressure > or =30/85 mmHg) and fasting glycemia > or =5.6 mmol/L (previously 6.1). IDF focuses on central obesity defined as waist circumference, taking into consideration sex and ethnic group specificities, with the presence of at least two additional factors (dyslipoproteinemia, hypertension, or increased fasting glycemia - all criteria virtually the same as in NCEP definition). Both IDF and NCEP define abdominal obesity by waist circumference, taking account of sex differences, and, in case of IDF, ethnic ones as well. The idea is to identify the simplest measure to indirectly determine the accumulation of visceral fat, which is, contrary to subcutaneous fat, a significant cardiovascular risk factor. However, waist circumference as the only criterion seems to be less specific than the waist-to-hip circumference ratio, which defines the risk more specifically and also better reflects insulin resistance. There is broad discussion as to whether the term metabolic syndrome contributes to the identification of persons at risk of cardiovascular disease better than its components, and, if so, which is the right set of components. It is being recommended that the discussion on the metabolic syndrome be limited to persons without diabetes or already diagnosed cardiovascular disease, as the primary goal for these individuals is to prevent these diseases. It has already been shown that this was possible, primarily by intensive change in lifestyle - healthy diet and exercise. In conclusion, further basic research is necessary to explain the pathophysiologic mechanisms, which might serve to develop new therapies. Moreover, epidemiological and public health aspects are extremely important in the creation of a prevention program. Preliminary results of the Croatian Health Survey (2003) indicate that the metabolic syndrome according to the IDF criteria is present even in the youngest age group, with expected age-dependent increase in both men and women. This is even an underestimate since in this survey only blood pressure and waist circumference were actually measured, and data on dislipidemia and blood glucose were based on a questionnaire. It is already obvious that a wide action with two main goals aimed primarily at the youngest population is necessary: an increase in regular physical activity and the promotion of healthy and energy-adequate diet in the population at large.
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PMID:[Metabolic syndrome: what, why, how and who?]. 1762 11

The metabolic syndrome (also referred to as syndrome X or the insulin resistance syndrome) has emerged as an important cluster of risk factors for atherosclerotic disease. Patients with the syndrome also are at increased risk for developing type 2 diabetes mellitus. Common features are central (abdominal) obesity, insulin resistance, hypertension, and dyslipidemia. Weight reduction deserves first priority in individuals with abdominal obesity and the metabolic syndrome. Both weight reduction and maintenance of a lower weight are best achieved by a combination of reduced caloric intake and increased physical activity. Dietary patterns close to the Mediterranean diet and rich in fruit and vegetables, and high in monounsaturated fats are negatively associated with features of the metabolic syndrome. Some recent studies dealing specifically with the effect of interventions on the resolution of the metabolic syndrome have demonstrated a 25% net reduction in the prevalence of the syndrome following lifestyle changes mainly based on nutritional recommendations. Similar rates of resolution have been obtained with drugs, such as rosiglitazone and rimonabant. The favourable benefit/hazard ratio makes Mediterranean-style diets particularly promising to reduce the cardiovascular burden associated with the metabolic syndrome.
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PMID:Mediterranean diet and the metabolic syndrome. 1787 92

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