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

Adipose tissue lipoprotein lipase (LPL) activity was determined in the abdominal and femoral regions in 25 pre- and 25 post-menopausal obese women, matched for body mass index and fat distribution. LPL activity was not different in pre- and post-menopausal women. Regional differences of the same magnitude were observed in pre- and post-menopausal women with femoral obesity. Such differences were not found in women with abdominal obesity either pre- or post-menopausal. Furthermore the abdominal/femoral ratio of LPL activity was positively correlated (P less than 0.05) to waist/hip ratio, independently of age, body mass index, fat cell size ratio and menopausal status. These data indicate that in obese women the regional differences in LPL activity are related to body fat distribution. The menopausal status does not seem to be a sufficient and necessary condition to abolish the typical female regional differences in LPL activity in adipose tissue from obese women.
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PMID:Regional differences in adipose tissue lipoprotein lipase activity in relation to body fat distribution and menopausal status in obese women. 323 65

Recent research has shown the marked differences in association with disease between obesity localized to the abdominal respectively to the gluteal-femoral regions. In this review systematic analyses were performed of the associations between obesity (body mass index, BMI) or abdominal obesity (increased waist-over-hip circumference ratio, WHR) on the one hand, and a number of disease end points, and their risk factors, as well as other factors on the other, WHR was associated with cardiovascular disease, premature death, stroke, non-insulin-dependent diabetes mellitus and female carcinomas. In contrast, BMI tended to be negatively correlated to cardiovascular disease, premature death, and stroke, but positively to diabetes. The established risk factors for these end points were found to correlate to WHR, while this was often not the case with BMI. BMI was positively correlated only to insulin, triglycerides and blood pressure. Together with diabetes mellitus, this seems to constitute a metabolic group of conditions which are thus associated with BMI. Androgens (in women), and perhaps cortisol, seem to be positively, and progesterone negatively correlated to WHR. The WHR was also positively associated with sick leave, several psychological maladjustments, psychosomatic and psychiatric disease. Attempts were made to interpret these findings. In a first alternative an elevation of FFA concentration, produced from abdominal adipose tissue, was considered to be the trigger factor for the pathologic aberrations associated with abdominal distribution of body fat. When obesity is added, the metabolic aberrations may be exaggerated. In a second alternative adrenal cortex hyperactivity was tested as the cause. When combined with the FFA hypothesis, this might explain many but not all of the findings. It seems possible to produce an almost identical syndrome in primates by defined experimental stress. Women with high WHR were found to have a number of symptoms of poor coping to stress. It was therefore suggested that part of the background to this syndrome might be a hypothalamic arousal syndrome developing with stress. It was concluded that obesity and abdominal distribution of adipose tissue constitute two separate entities with different pathogenesis, clinical consequences and probably treatment.
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PMID:The associations between obesity, adipose tissue distribution and disease. 329 56

Because recent knowledge indicates that the distribution of fat deposits in men may be a better predictor of cardiovascular disease than the degree of obesity alone, some risk factors for atherosclerosis were evaluated in 51 middle-aged men with non-insulin-dependent diabetes mellitus. Abdominal adiposity (waist/hip ratio, WHR) was related to parameters of metabolic control, lipid parameters, and known vascular complications in three different groups. In groups with abdominal obesity, mean annual hemoglobin A1 was significantly (P less than .01) higher than in patients without an abdominal fat distribution. Atherogenic index was significantly increased in the group with the highest WHR and high-density lipoprotein cholesterol (HDL-chol) levels were significantly decreased in both groups with upper-body fat distribution. The frequency of peripheral vascular disease, coronary ischemic heart disease, and hypertension was most prominent in diabetic subjects with an abdominal fat mass distribution. A highly significant (P less than .001) correlation was present between WHR and HDL-chol and WHR and the total-cholesterol/HDL-chol ratio; this significant correlation remains after correction for body mass index. A similar correlation could be found between WHR and systolic and diastolic blood pressures. These results demonstrate an association of excess abdominal fat, even without manifest obesity, with worse diabetes metabolic control, cardiovascular complications, and blood lipid levels actually considered to play an important role in atherogenesis.
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PMID:Relationship of body fat distribution pattern to atherogenic risk factors in NIDDM. Preliminary results. 338 30

There is growing evidence that differences in fat distribution can be predictive for differences in the prevalence of metabolic disturbances, cardio-vascular disease, stroke and death, independent of commonly used indices of obesity. This study evaluates regional body fat distribution as a possible main reason for hypertension in obese and non-obese type II diabetics. 42% of normal weight diabetics with abdominal obesity are hypertensive versus 47% of obese diabetics; only 5% hypertension could be found when a lower body segment fat distribution is present. A significant (p less than 0.001) correlation exists between fat mass topography and both systolic (r = 0.49) and diastolic (r = 0.49) blood pressure. This correlation remains true after correction for body mass index and percent glycosylated hemoglobin. These results suggest that localization of fat in the upper body segment should be considered as a additive risk for hypertension.
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PMID:Hypertension in obese and non-obese non-insulin dependent diabetics a matter of regional adiposity? 341 Jan 53

Abdominal obesity is related to reduced plasma high-density lipoprotein (HDL) cholesterol, and both are associated with cardiovascular disease risk. We have observed that plasma membranes from abdominal subcutaneous adipocytes have a greater HDL binding capacity than omental fat cell plasma membranes. The present study examined whether these binding characteristics could be due to differences in fat cell size or cholesterol concentration between the two adipose depots. Abdominal subcutaneous and deep omental fat were obtained from massively obese patients at surgery. Subcutaneous abdominal fat cells were significantly larger and their cellular cholesterol content greater than omental adipocytes. The uptake of HDL by collagenase-isolated fat cells was studied by incubating the cells for 2 h at 37 degrees C with 10 micrograms/ml 125I-HDL2 or 125I-HDL3. In both depots, the cellular uptake of 125I-HDL2 and 125I-HDL3 was specifically inhibited by addition of 25-fold excess unlabeled HDL and a close correlation was observed between the cellular uptake of 125I-HDL2 and 125I-HDL3. In obese patients, the uptake of 125I-HDL was higher in subcutaneous cells than in omental cells [5.85 +/- 0.53 vs. 2.74 +/- 0.30 pmol X 2 h-1. (10(6) cells)-1]. The cellular 125I-HDL uptake was significantly correlated with adipocyte size and fat cell cholesterol content but not with adipocyte cholesterol concentration. These results suggest that the higher HDL uptake observed in subcutaneous cells compared with omental cells in obesity is the result of differences in adipocyte size rather than differences in the cholesterol concentration (cholesterol-to-triglyceride ratio).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional variation in HDL metabolism in human fat cells: effect of cell size. 357 14

In over 30 years of surveillance of 2873 women, 574 developed initial clinical manifestations of CHD. A number of antecedent metabolic risk factors proved atherogenic, including blood lipids, glucose tolerance, uric acid, and menopause. Serum total cholesterol predicts as strongly in women as in men. The predictive power of cholesterol is strengthened when the total cholesterol is partitioned into its atherogenic LDL and protective HDL fractions. Contrary to the case in men, triglyceride may be a contributor to risk in older women. A total-to-HDL cholesterol ratio exceeding 7.5 equalizes the risk in men and women. Impaired glucose tolerance also eliminates the female CHD risk advantage over men, conferring a three-fold increased risk. Serum uric acid, although lower in women than in men, is equally predictive in the sexes. Central obesity confers an increased CHD risk in women and predisposes to diabetes, hyperuricemia, hypertension, and an unfavorable LDL/HDL cholesterol ratio. A combination of obesity, low HDL cholesterol, and impaired glucose tolerance predisposes especially. Age-adjusted risk of CHD is increased two- to threefold compared to pre menopausal women, even when induced surgically without removing the ovaries. It is not clear whether post menopausal estrogen replacement eliminates this excess risk. Fibrinogen is higher in women than in men, and is increased with hypertension, diabetes, hypercholesterolemia, high hematocrit, and cigarette smoking. At any level of multivariate risk, fibrinogen added to the CHD risk in women.
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PMID:Metabolic risk factors for coronary heart disease in women: perspective from the Framingham Study. 360

Waist-hip circumference ratio (WHC ratio) and body mass index (BMI) were calculated from measurements of a semi-random, age-stratified sample of 4349 British men, aged 20-64 years, body weight 75.6 +/- 11.6 kg (mean +/- s.d.) and BMI 24.7 +/- 3.4 kg/m2. The mean WHC ratio was 0.89 +/- 0.06; it increased with age and overweight separately and in combination, R2 = 47 per cent. BMIs greater than or equal to 30 were found in 7 per cent of the sample and WHC ratios greater than or equal to 1 in 4 per cent of the sample. Forty-seven per cent of these latter individuals also had BMI greater than or equal to 30, but only 28 per cent of individuals with BMI greater than or equal to 30 had WHC ratios greater than or equal to 1. These indices suggest that in men abdominal obesity and whole-body obesity are usually separate conditions and that abdominal obesity is less common than obesity.
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PMID:Waist-hip circumference ratio and its relation to age and overweight in British men. 372 6

The original notion that obesity is associated with disease and premature death was obtained from insurance statistics, which have been rightfully criticized for representing selected populations. In prospective, epidemiological studies a long period of observation on a large number of subjects is needed before obesity can be recognized as a risk factor for cardiovascular disease in spite of the fact that well-known risk factors for such disease are prevalent in obesity populations. This apparent paradox may be explained by the possibility that the risk of getting cardiovascular disease is present mainly in a subgroup of the total obese population. Such a subgroup might be characterized by the distribution of adipose tissue. Indeed abdominal obesity has been demonstrated consistently to be strongly associated with risk factors for cardiovascular disease in cross-sectional investigations of older and more recent dates. Several prospective longitudinal, epidemiological studies in both men and women have shown that abdominal obesity is associated with an increased risk of getting ischemic heart disease, stroke and death, independent of the total degree of obesity. The findings from these recent prospective studies, supported by previous unanimous cross-sectional studies as well as the fact that reasonable potential explanations for the statistical associations have been suggested, now seem to allow the conclusion that abdominal obesity should even be treated when present to a very limited extent. In such subjects, exclusion of conditions complicating obesity should also be performed vigorously. Abdominal obesity can be diagnosed by very simple means: measuring the abdominal circumference in relation to hip circumference.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Obesity and the risk of cardiovascular disease. 389 10

Recent studies have shown that adipose tissue metabolism varies in different regions. Thus, hormonal responsiveness and sensitivity to both lipolytic and anti-lipolytic agent is increased in abdominal as compared to femoral cells. Abdominal obesity is also associated with greater aberrations in metabolism than peripheral obesity. The increased lipolytic response in abdominal fat cells may lead to higher FFA concentrations, which may attenuate both glucose uptake and insulin clearance by the liver.
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PMID:Regional differences in adipocyte metabolism and possible consequences in vivo. 390 44

Obesity is a heterogeneous group of disorders in terms of etiology; time of development; adipose tissue characteristics; metabolic abnormalities; and associated morbidity and mortality from coronary disease. The typical patient at risk for coronary artery disease in middle age develops abdominal obesity with hypertrophic fat cells in young adulthood, has hypertension, hyperglycemia, hypertriglyceridemia, hypercholesterolemia, and decreased high density lipoprotein (HDL)-cholesterol levels. Two common genetic metabolic disorders--noninsulin-dependent diabetes and familial combined hyperlipidemia--both conform to the prototype, accounting perhaps for a substantial amount of the coronary artery disease associated with obesity.
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PMID:Obesity and common genetic metabolic disorders. 406 24


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