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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Muscle and fat development are regulated by opposite and also cooperating factors. Adipo-muscular ratio is the result of those forces. The need of a determined fat mass and of its corollary a determined muscle mass is an important physiologic parameter. Sexual differentiation is the main factor adipo-muscular ratio. Feminine fat is twice as big as masculine fat: it predominates in the lower body, masculine fat in the upper body. Brachio-femoral adipo-muscular ratio is, among others, a good index of fat sexual differentiation. Android obesity, predominating in both sexes in the upper body, is, with genetic predispositions, the main factor of non insulin dependent diabetes carbohydrate sensitive hyperlipoproteinemia, hyperuricemia, atherosclerosis. Easy determination on fat topography before the age of 30 is, particularly in women, the best tool for an efficacious prophylaxis of obesity's metabolic complications.
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PMID:[Sexual differentiation of the adipose tissue-muscle ratio. Its metabolic impact]. 276 1

Android obesity is associated with metabolic disorders, but the causality of this relationship remains unclear. We investigated the association of body mass index (BMI) and waist-to-hip ratio (WHR) with hormones, glucose tolerance, insulin sensitivity, serum lipoproteins, and the serum activity of hepatic enzymes in 40 healthy premenopausal women (BMI 19.2-46.1, mean 32.6 +/- 1.3 kg/m2; WHR 0.68-1.01, mean 0.82 +/- 0.02). BMI correlated with WHR (r = 0.52, P < 0.01). After correction for WHR, BMI was negatively correlated with high-density lipoprotein cholesterol and positively with total and very low density lipoprotein triglycerides, insulin sensitivity, blood glucose, serum insulin and glucagon. After adjustment for BMI, WHR was significantly associated with high-density lipoprotein cholesterol, total and very low density lipoprotein triglycerides, and the serum activities of hepatic enzymes but not with insulin sensitivity, blood glucose, serum insulin, or glucagon. According to these results, body fat distribution assessed by WHR is related to hypertriglyceridemia and alterations in hepatic function such as a fatty liver. WHR is not primarily related to glucose metabolism in healthy premenopausal women without preexisting metabolic disorders such as glucose intolerance. Therefore the observable association between android obesity and manifest impairment in glucose metabolism may develop secondarily during persisting hyperinsulinemia, which itself is primarily related to obesity. Thus an android body fat distribution may rather be an accompanying feature than a predictor of impaired glucose tolerance and insulin resistance.
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PMID:The waist-to-hip ratio corrected for body mass index is related to serum triglycerides and high-density lipoprotein cholesterol but not to parameters of glucose metabolism in healthy premenopausal women. 831 84

There are several types of obesity, and the metabolic conditions associated with these phenotypes are also heterogeneous. Obesity of the male (android) type shows a dominant visceral and upper thoracic distribution of adipose tissue, whereas in the feminine (gynecoid) type adipose tissue is found predominantly in the lower part of the body (hips and thighs). Android obesity is clearly a cardiovascular risk factor, more so than gynecoid obesity. Hereditary factors contribute significantly to the occurrence of this pathology in families, although environmental factors play a role in its development. Android obesity is associated with metabolic anomalies which also characterize the syndrome X: resistance to insulin, arterial hypertension and dyslipidemia. The predisposition of individuals with android obesity to become diabetic rests in part on genetic and in part on environmental factors. Hyperinsulinemia and a high flux of free fatty acids act at the level of liver and endocrine pancreas to increase resistance to insulin and to decrease insulin secretion, two determining factors for type II diabetes. Other functional anomalies have been involved to explain android obesity such as dysregulation of adrenocortical and sexual steroids or a global derangement of stress mechanisms. No significant proof, however, seems to support either one of these hypotheses.
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PMID:[Android-type obesity and gynecoid-type obesity]. 899 75

Obesity stands as a public health issue. Obesity prevalence is increasing throughout every industrialized country. Android obesity is linked with an increased cardiovascular mortality and with type 2 diabetes mellitis, thus calling for an early management of this disease. Several studies showed a significant association between an android fat distribution and an increased cortisol secretion, raising the still debated question of a causal relationship between the development of android obesity and hypercorticism. Moreover, android obese subjects exhibit reduced plasma testosterone and growth hormone levels, meaning complex hormonal abnormalities in these subjects. Current hypotheses suggest that android fat distribution depends on the association of these hormonal abnormalities. Android obese patients have supranormal free fatty acid plasma concentrations. Visceral fat tissue, through its portal drainage, could be an important source for free fatty acids that may exert complex metabolic effects: involvement in hepatic lipogenesis, increase in hepatic neoglucogenic flux, reduction in insulin metabolic clearance and involvement in peripheral insulin resistance through a competition mechanism described by Randle. Technics in vitro (isolated adipocytes) and in vivo in human (labelled fatty acid flux) showed that visceral fatty acid flux was increased in obese patients and subcutaneous adipose tissue, as opposed to common opinion, was also involved in free fatty acid pool in obese patients. Thus, visceral obesity and diabetes could be linked through an enhanced fatty acid availability from adipose tissues (visceral and subcutaneous) in otherwise genetically type 2 diabetes-prone individuals.
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PMID:[Metabolic difference between visceral fat and subcutaneous abdominal fat]. 1094 44

Excess of adipose tissue may affect the reverse cholesterol transport mediated by high-density lipoprotein (HDL). Impairments in this system may be one possible factor favoring atherosclerosis development in obesity. To investigate if gender and regional fat mass distribution independently influence reverse cholesterol transport (RCT), we studied in vitro the capacity of serum to promote the cell cholesterol efflux. Measurements were performed both in the fasting state and in the postprandial state, a setting known to stimulate cholesterol transport and altered in obesity. Thirteen obese women with an android phenotype, waist-to-hip ratio (WHR): 0.98 to 0.85 and 51 normal-weight subjects: 25 women and 26 men, with a similar WHR range: 0.96 to 0.67, were recruited. All the participants were normolipoproteinemic in the fasting state and were given an oral fat load. Blood samples were taken before giving the oral fat load and after every 2 hours. The measurements of the ability of serum to promote cholesterol efflux from cells were performed using 3H-cholesterol labeled Fu5AH hepatoma cells in the fasting state 6 and 8 hours after the lipid rich meal. Incremental serum triglyceride (TG), area under the curve (iAUC) and AUC of retinyl palmitate (RP) for the obese women and nonobese subjects were similar. Basal cholesterol efflux was reduced in obese women compared with normal-weight women (26.75% +/- 3.1% v 30.81% +/- 4.2%, P =.004). However, the magnitude of cholesterol efflux promoted by whole serum increased similarly in all the groups. In the subjects with similar WHR, no gender difference was observed in the postprandial TG response and in the first step of RCT. Multivariate regression analyses indicated that plasma HDL-cholesterol (HDL-C) concentration is the best predictor of cholesterol efflux in the fasting state with an independent mild additive effect of WHR. Conversely, postprandial efflux appeared to be mostly related to the WHR with a mild additive effect of HDL-C. Our results indicate that alterations in the first step of RCT can occur in normolipidemic obese subjects and are tightly associated with the abdominal distribution of fat mass. Android obesity in women brings them to the level of men with respect to RCT.
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PMID:Basal and postprandial serum-promoted cholesterol efflux in normolipidemic subjects: Importance of fat mass distribution. 1169 52

The prevalence of obesity is increasing rapidly in most industrialized countries and it is known that obesity is associated with increased risk of cardiovascular morbidity and mortality. Commonly, obesity is defined by the Body Mass Index (BMI). However, BMI fails to consider body fat distribution. The relationship between the risk of metabolic-cardiovascular diseases and body fat distribution indices, rather than measures of the degree of body fatness as expressed by BMI, has long been recognized. Clinical and epidemiological research has found waist circumference to be the best anthropometric indicator of both total body fat and intra-abdominal fat mass. Android obesity is associated with metabolic syndrome and increased cardiovascular risk through molecular mechanisms possibly linking the metabolic syndrome to hemostatic and vascular abnormalities. Obesity guidelines suggest the need for weight reduction using behavioural change to reduce caloric intake and increasing physical activity. A realistic goal for weight reduction is to reduce body weight by 5% to 10% over a period of 6 to 12 months. Combined intervention of a low calories diet, increased physical activity, and behaviour therapy provides better outcomes for long-term weight reduction and weight maintenance than programs that use only one or two of these modalities. The anorexiant drugs affect neurotransmitters in the brain. The sibutramine has norepinephrine and serotonin effects. Orlistat has a different mechanism of action: the reduction of fat absorption. Recently, the blockade of the endocannabinoid system with rimonabant may be a promising new strategy.
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PMID:[What do we know about obesity?]. 1761 88