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

This study was designed to evaluate the role of fasting serum insulin and plasma renin activity in obesity-induced hypertension. In view of this, plasma catecholamines, fasting serum insulin (IRI), urinary sodium excretion (NaU), plasma renin activity (PRA), and plasma aldosterone (PA) levels were assessed in young (age less than 40 years) normotensive (n = 27) and hypertensive (n = 14) subjects with central obesity and in lean normotensives (n = 20). Central obesity was evaluated by waist-to-hip ratio (WHR) according to the indication of the Italian Consensus Conference of Obesity. PRA, PA, IRI, and plasma norepinephrine levels were significantly (P < .05) higher in both obese groups than in lean normotensives. PRA was significantly (P < .05) higher and NaU was significantly (P < .05) lower in obese hypertensives than in obese normotensives. Diastolic blood pressure correlated directly with WHR and PRA in normotensive and hypertensive obese subjects and with IRI but only in normotensive obese subjects. Multiple regression analysis indicated that diastolic blood pressure values increased with WHR (P < .05), IRI (P < .005), and PRA (P < .002), but not with body mass index, NaU, and norepinephrine levels. Our results indicated that increased PRA could play an important role in the development of hypertension in subjects with central obesity.
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PMID:Central obesity and hypertension. Relationship between fasting serum insulin, plasma renin activity, and diastolic blood pressure in young obese subjects. 803 46

The topographic specificity of upper body obesity is known to be at the origin of a series of metabolic complications. In contrast to this negative effect, women with abdominal obesity usually can lose more body weight than women with gluteal-femoral obesity. In order to find some contributive explanations for this effect, we studied resting metabolic rate (RMR) and glucose-induced thermogenesis (GIT) in both types of obesity. Since upper body obesity is characterized by androgen excess, a relationship between body fat distribution, sex hormones, RMR and indices of thermogenesis was studied. Of 39 obese women who were recruited (mean age: 32.4 +/- 9.3 years), 30 were compared for analysis. Upper body obesity (waist-to-hip ratio (WHR): 0.84 +/- 0.02; body mass index (BMI) 36.2: 36.2 +/- 6.0) is not characterized by differences in RMR, whereas glucose-induced thermogenesis is significantly higher in this subgroup (P < 0.008), expressed as percentage increase above RMR (18.3 +/- 8.5 vs. 11.9 +/- 3.6%) or as percentage of metabolisable energy intake (8.2 +/- 3.3 vs. 5.8 +/- 2.3%). Correlation coefficient data show that GIT determinants are closely related to WHR (r = 0.43; P < 0.01) and not to BMI. Resting metabolic rate, both in absolute terms and corrected for fat-free mass (FFM), is not related to indices of androgenicity, but is negatively related to serum oestradiol levels; this negative relationship with oestradiol disappears when RMR is corrected for both fat mass (FM) and FFM. GIT parameters are not related to free testosterone or oestradiol, regardless of the phase of the menstrual cycle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sex hormones, body fat distribution, resting metabolic rate and glucose-induced thermogenesis in premenopausal obese women. 806 27

Upper-body obesity is an important risk factor for developing non-insulin dependent diabetes. To investigate the possibility that a lipolysis defect is present in this form of obesity, we examined the adrenergic regulation of lipolysis in abdominal subcutaneous fat cells from 25 women with upper-body obesity and 24 non-obese women. Lipolytic noradrenaline sensitivity (but not the maximum rate of lipolysis) was reduced by 10-fold in obese women (p < 0.01). The noradrenaline resistance could be ascribed to a 10-fold decrease in lipolytic beta 2-adrenoceptor sensitivity (p < 0.01). The lipolytic sensitivity of beta 1- and alpha 2-adrenergic receptors was normal in the obese women. A 70% reduction in the cell surface density of beta 2-adrenoceptors was observed compared to the control subjects (p < 0.01). However, beta 1-receptor density as well as steady-state mRNA levels for beta 1- and beta 2-receptors were normal in obese women. Lipolytic noradrenaline sensitivity correlated inversely with BMI (adjusted r2 = 0.76 together with fat cell volume in stepwise regression analysis). The fasting plasma level of free cortisol was 30% lower in obese compared to non-obese women (p < 0.05) but obesity did not influence resting plasma catecholamine levels. Thus, lipolytic catecholamine resistance is present in abdominal obesity, due to low density of beta 2-adrenoceptors, which in its turn may be caused by a post-transcriptional defect in beta 2-receptor expression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Catecholamine resistance in fat cells of women with upper-body obesity due to decreased expression of beta 2-adrenoceptors. 774 23

We investigated the feedback inhibition of insulin and glucagon secretion during euglycemic-hyperinsulinemic clamp at about 350 pmol/l in 16 patients with abdominal obesity [8 with normal glucose tolerance (oNGT), 8 with impaired glucose tolerance (oIGT)] and 8 normal-weight subjects matched for age, sex and blood pressure. In oNGT and oIGT, fasting plasma C-peptide levels were twice those in the controls (962 +/- 51 and 915 +/- 85 vs 439 +/- 28 pmol/l, P < 0.001) and their suppression was lower than in the controls, both in absolute terms (155 +/- 19 and 185 +/- 17 vs 274 +/- 18 pmol/l, P < 0.001) and as a percentage decline from basal levels (16 +/- 2% and 21 +/- 2% vs 63 +/- 2%, P < 0.001). Fasting plasma glucagon levels were similar in the patients and in the controls, but were less suppressed during clamp in oNGT and oIGT, both in absolute terms (7.0 +/- 0.9 and 5.6 +/- 0.6 vs 13.2 +/- 1.2 pmol/l, P < 0.001) and as a percentage change from basal levels (23 +/- 3% and 19 +/- 2% vs 44 +/- 4%, P < 0.001). These results suggest that the insulin feedback on B and A cells is impaired in abdominal obesity, and that this defect is of similar degree in oNGT and oIGT. These alterations could be implicated in the pathogenesis of hyperinsulinemia in obesity.
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PMID:Feedback inhibition of insulin and glucagon secretion by insulin is altered in abdominal obesity with normal or impaired glucose tolerance. 811 Oct 76

Noninsulin-dependent diabetes mellitus and postmenopausal breast cancer share a number of risk factors, including obesity, increased waist-to-hip ratio, and a positive family history. If risk for these diseases is mediated through a familial tendency for abdominal obesity, then one might expect to see familial clustering of both diseases. We analyzed data from a prospective cohort study of 41,837 Iowa women age 55-69 years. Diabetes was not associated with incidence of breast cancer [relative risk (RR) = 0.97]. The association between family history of breast cancer and breast cancer incidence, however, was slightly modified by individual history of diabetes: a positive family history of breast cancer in the absence of baseline diabetes was associated with a relative risk of 1.36 [95% confidence interval (CI) = 1.08-1.70], whereas the presence of both factors was associated with a RR of 1.87 (95% CI = 0.93-3.76). Adjustment for waist-to-hip ratio greatly diminished this difference. Conversely, a family history of breast cancer was associated with a RR of 5-year diabetes mortality of 1.94 (95% CI = 1.17-3.24) that persisted after stratification by tertile of waist-to-hip ratio. No clear association of family history of breast cancer and waist-to-hip ratio for self-reported diabetes incidence was evident. These data are indicative of a complex interrelation between waist-to-hip ratio, familial predisposition, diabetes, and breast cancer.
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PMID:Does body fat distribution promote familial aggregation of adult onset diabetes mellitus and postmenopausal breast cancer? 811 67

Abdominal obesity and hyperinsulinemia are associated with abnormalities in lipid metabolism and are important risk factors for coronary artery disease. Because hyperinsulinemia frequently accompanies abdominal obesity, it is unclear whether each is independently related to lipid abnormalities. Dietary saturated fat may influence these associations since it is associated with elevated lipid levels, obesity and hyperinsulinemia. Abdominal obesity (indexed as abdomen-to-hip circumference ratio), serum insulin level and dietary saturated fat intake were examined in relation to serum levels of lipids and lipoproteins in 878 male participants of the Normative Aging Study. Abdomen-to-hip ratio and insulin level were inversely related to high density lipoprotein cholesterol (HDL-C) (r = -0.17 and -0.21, respectively), and positively related to triglycerides (r = 0.25 and 0.36, respectively). Saturated fat intake was positively related to body mass index (r = 0.20), abdomen-to-hip ratio (r = 0.13), and insulin level (r = 0.10). In multiple linear regression models, abdomen-to-hip ratio was positively related to triglycerides and low density lipoprotein cholesterol (LDL-C) after adjusting for the effects of body mass index, alcohol intake, age, cigarette smoking and physical activity level, but was not significantly related to HDL-C. When serum insulin level was included as a covariate, abdomen-to-hip ratio remained significantly related to LDL-C and triglycerides, although its relationship with triglycerides was attenuated. Insulin level remained inversely related to HDL-C and triglycerides in multivariate models which adjusted for the effects of abdomen-to-hip ratio and BMI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The relationships of abdominal obesity, hyperinsulinemia and saturated fat intake to serum lipid levels: the Normative Aging Study. 818 10

Individuals with abdominal obesity are at increased risk for the development of coronary artery disease (CAD). This study examines whether an abdominal fat distribution, indexed by the waist to hip ratio (WHR), is associated with an atherogenic lipoprotein lipid profile independent of the degree of obesity (percent body fat) and maximal aerobic capacity (VO2max) in 127 older (60 +/- 8 years, mean +/- SD) normotensive, nonsmoking, nondiabetic men. Compared to men with WHR below the population mean (< 0.96, low WHR), men with high WHR (> 0.96) had higher triglycerides (TG) (124 +/- 47 vs. 93 +/- 48 mg/dl, p < 0.001) and lower high density lipoprotein cholesterol (HDL-C) (34 +/- 7 vs 41 +/- 9 mg/dl, p < 0.001) levels with no difference in low density cholesterol (LDL-C) levels. Plasma TG levels were positively associated with both percent body fat (r = 0.50, p < 0.0001) and WHR (r = 0.49, p < 0.0001), and negatively with VO2max (r = -0.36, p < 0.0001), whereas plasma HDL-C levels were negatively associated with percent body fat (r = -0.50, p < 0.0001) and WHR (r = -0.54, p < 0.0001), and positively with VO2max (r = 0.45, p < 0.0001). Independent relationships between WHR and both plasma TG (r = 0.30, p < 0.001) and HDL-C (r = -0.34, p < 0.0001) remained after correction for both percent body fat and VO2max. Using analysis of covariance, the differences in TG and HDL-C between groups remained after adjustment for percent body fat and VO2max. These results suggest that in older men, an abdominal distribution of body fat, independent of both percent body fat and VO2max, is associated with elevated TG and low HDL levels, thus increasing the risk for CAD.
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PMID:Adverse effects of abdominal obesity on lipoprotein lipids in healthy older men. 822 38

The relationship between obesity and prevalence of dyslipidemia is well known. Recent studies affirm that differences in fat distribution can be predictive for differences in the prevalence of metabolic disturbances and cardiovascular disease independently of the BMI, presently the most common index of obesity. In order to verify whether body fat distribution can be associated with a higher risk of atherosclerosis, we have evaluated in a group of obese women the eventual presence of endocrine and metabolic diseases. Assessing regional fat distribution, the waist/hip ratio has been shown to be more closely correlated with these diseases than BMI. We have studied two groups of 10 women, comparable for age and BMI: group A aged 45.8 +/- 6.9 years with a BMI of 35.6 +/- 2.8 kg/m2; group B aged 48.3 +/- 3.6 years with a BMI of 38.5 +/- 2.8 kg/m2. The women were divided according to the waist-hip ratio, which was calculated by measuring the circumference of the waist, namely the smallest circumference between the xiphoid and the umbilicus, and the circumference of the hips at the point of the maximum protuberance of the buttocks. The cut-off value for the waist/hip ratio was considered as 0.80 for the reason that this variable is the most accurate cut-off value for abdominal obesity: for group A 0.76 +/- 0.02; for group B 0.89 +/- 0.02 (p < 0.01). All the women were healthy. None of them was in therapy with any kind of drugs, nor was there any restriction to diet. Nobody was a smoker, neither did anyone drink alcoholic beverages.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Transverse study of obesity: distribution of adipose tissue and correlated pathology]. 823 18

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

The hypothesis that a causal relationship exists between insulin resistance and atherogenesis was first proposed over 23 years ago, and has given rise to a vast literature. Biological plausibility has been lent to the hypothesis by studies in which insulin has produced some effects in cell and tissue culture, and in vivo in arterial tissue, consistent with our understanding of the pathogenesis of atherosclerosis. Clinical studies demonstrating a complex interrelationship between insulin resistance-hyperinsulinaemia and established risk factors for CHD--hypertension, hypertriglyceridaemia, low HDL cholesterol levels and abdominal obesity--are reviewed. A review of the studies examining an independent association between hyperinsulinaemia and coronary heart disease is presented. Cross-sectional studies in both the general population and diabetes support the relationship; however, prospective studies in the general population provide limited and inconsistent support for this hypothesis and highlight the confounding effects of blood pressure, dyslipidaemia and obesity on the effects of hyperinsulinaemia. In subjects with NIDDM and impaired glucose tolerance, prospective studies have not shown a deleterious effect of insulin treatment per se, nor have they consistently shown a significantly increased risk for those with higher endogenous insulin levels. The therapeutic implications of the evidence to date are less complex and involve weight reduction by diet and exercise, the lowering of elevated blood pressure with metabolically neutral agents, the judicious use of lipid lowering drugs and, in diabetes, the use of insulin where clinically indicated.
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PMID:Relationship between insulin resistance and coronary heart disease in diabetes mellitus and the general population: a critical appraisal. 830 14


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