Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased abdominal obesity has been related to lower insulin sensitivity (SI), independent of overall obesity, but it has been suggested that this relationship may be weaker in non-whites. In the Insulin Resistance and Atherosclerosis Study (IRAS), SI was estimated using a minimal model analysis of the frequently sampled intravenous glucose tolerance test in 1,625 men and women aged 40-69 years. Subjects included African-Americans, Hispanics, and non-Hispanic whites from Oakland and Los Angeles, CA, San Antonio, TX, and the San Luis Valley, CO. Minimum waist circumference was significantly (P = 0.0001) associated with SI after adjusting for age, sex, height, BMI, glucose tolerance status, ethnicity, and clinic. This relationship was significantly (P = 0.0001) stronger in subjects with normal glucose tolerance (NGT) (beta = -0.030, P = 0.0001) than in those with impaired glucose tolerance (IGT) (beta = -0.010, P = 0.02; NIDDM: beta = -0.013, P = 0.0001). There were no significant ethnic differences in effect size across the spectrum of glucose tolerance. Waist circumference was also positively related to fasting insulin, an indirect measure of insulin sensitivity, in NGT (P = 0.0001), IGT (P = 0.0003), and NIDDM (P = 0.0002). The waist-fasting insulin relationship was significantly weaker in African-Americans, relative to non-Hispanic whites, in NGT and IGT (tests of statistical interaction: P = 0.04 and P = 0.02, respectively). In general, these patterns were similar in models specifying waist-to-hip ratio (WHR), rather than waist circumference, as the independent variable. While some ethnic variability exists, a negative relationship between abdominal obesity and insulin sensitivity was confirmed for all three ethnic groups across the spectrum of glucose tolerance.
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PMID:Insulin sensitivity and abdominal obesity in African-American, Hispanic, and non-Hispanic white men and women. The Insulin Resistance and Atherosclerosis Study. 886 60

Although a strong genetic susceptibility has been established for NIDDM and a maternal transmission of the disease predominates in some populations, a relationship between parental diabetes status and metabolic abnormalities in nondiabetic offspring has not been shown in humans. To address this question, we studied 2,152 first-degree relatives of patients with NIDDM (FH+) and 528 age- and weight-matched spouses without a family history of NIDDM (FH-) in Western Finland (the Botnia study). A subset of the subjects underwent a euglycemic insulin clamp combined with indirect calorimetry to measure insulin sensitivity and energy expenditure. Despite similar amounts of total body fat, persons with a family history of NIDDM had a greater waist-to-hip ratio (WHR) than spouses without a family history of diabetes (P < 0.003). They also had a decreased resting metabolic rate (P = 0.005), but this difference disappeared when adjusted for the difference in WHR. Insulin-stimulated glucose metabolism (P = 0.002), particularly nonoxidative glucose metabolism (P = 0.009), was reduced in FH+ compared with FH- subjects, and this difference remained after adjustment for WHR. A parental history of NIDDM influenced the insulin response to the oral glucose load, with male offspring of diabetic mothers showing the lowest insulin values (P = 0.011). Moreover, a parental effect was also observed on HDL and HDL2 cholesterol concentrations with female offspring of diabetic mothers showing lower values than female offspring of diabetic fathers (both P < 0.002). We conclude that abdominal obesity, insulin resistance, and decreased resting metabolic rate are characteristic features of first-degree relatives of patients with NIDDM and that the decrease in resting metabolic rate is partially related to the degree of abdominal obesity. A sex-specific paternal effect was observed on insulin and HDL cholesterol concentrations. Therefore, one has to consider the possibility of unprecedented maternal or paternal inheritance of different NIDDM phenotypes.
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PMID:Metabolic consequences of a family history of NIDDM (the Botnia study): evidence for sex-specific parental effects. 886 65

The results of recent studies suggest that a relative hypogonadism in men is associated with several established risk factors for prevalent diseases. Therefore, we determined total and free testosterone, luteinizing hormone (LH), and sex-hormone binding globulin (SHBG) in a cohort of randomly selected men (n = 659) at 67 years of age. These data were analyzed cross-sectionally in relation to blood glucose and serum insulin, which were measured while fasting and after an oral glucose tolerance test, in addition to plasma lipids and blood pressure. The data were also analyzed in relation to impaired glucose tolerance (IGT) and diabetes, which were discovered at examination or earlier diagnosis. Risk factors for the development of diabetes up to 80 years of age were analyzed with univariate and multivariate statistics. Total and free testosterone and SHBG concentrations correlated negatively with glucose and insulin values; total testosterone and SHBG, with triglycerides; and SHBG, with blood pressure (from P < 0.05 to P < 0.01). Men with IGT or newly diagnosed diabetes had higher BMI values (26.2 +/- 0.31 and 27.0 +/- 0.59 [mean +/- SE], respectively) and waist circumference (99.0 +/- 1.03 and 100.5 +/- 1.57) than nondiabetic men (BMI, 25.1 +/- 0.14; waist circumference, 95.4 +/- 0.47; P < 0.05), indicating abdominal obesity. Such men and men with previously diagnosed diabetes had, in general, lower total and free testosterone and SHBG levels, while those for LH were not different. In multivariate analyses that included BMI, waist-to-hip ratio, total and free testosterone, and SHBG, the remaining independent predictors for the development of diabetes were low total testosterone (P = 0.015) and, on the borderline, low SHBG (P = 0.053). In relation to nondiabetic men, the risk ratio for mortality, myocardial infarction, and stroke increased gradually and significantly from 1.18 to 1.68, from 1.51 to 1.78, and from 1.72 to 2.46 in men with IGT, newly diagnosed diabetes, and previously known diabetes, respectively. It was concluded that low testosterone and SHBG concentrations in elderly men are associated with established risk factors for diabetes and in established diabetes. Moreover, low testosterone levels independently predict the risk of developing diabetes. In different degrees of expression, the diabetic state predicts strongly (and gradually mortality from) myocardial infarction and stroke. It has been suggested that a relative hypogonadism might be a primary event, because other studies have shown that testosterone deficiency is followed by insulin resistance, which is ameliorated by testosterone substitution. The data suggest that the relative hypogonadism involved might be of both central and peripheral origin.
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PMID:The pituitary-gonadal axis and health in elderly men: a study of men born in 1913. 886 67

The aim of this study was to evaluate the alterations of the lipoprotein composition and their relation with the insulin-resistance and/or hyperinsulinemia in non diabetic obese patients. Twenty-two no obese(13 women and 9 men) and 30 obese patients (BMI > 30) were studied, who were divided into two groups according to the total lipid levels. The first group was formed by 18 obese patients (10 women and 8 men) with normal serum cholesterol (Chol) concentration < 200 mg/dL and triglycerides (TG) < 150mg/dL (NO), while the second group were formed by 12 obese patients (3 women and 9 men) with elevated Chol level > 200mg/dL and/or TG > 150 mg/dL (HO). A clinical and anthropometric examination was performed to each patient, as well as a glucose tolerance test, including serum glucose and insulin determinations. Likewise, the plasma lipoproteins (VLDL, LDL, HDL2 and HDL3) were isolated by ultracentrifugation and their cholesterol and triglycerides content were determined by enzymatic methods. In this report, we demonstrate the existence of compensatory basal hyperinsulinemia in men and women on both obese patients populations as well as alterations in the lipoprotein composition, mostly a TG overload even on NO. On the other hand, the presence of lipids and lipoproteins modification were obvious in those patients with abdominal obesity, on whom the hyperinsulinemia was more evident, which could be related with the high risk of cardiovascular disease in this kind of patients.
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PMID:[Qualitative and quantitiative differences in the plasma lipoproteins of obese, hyperlipidemic or normolipidemic men and women]. 892 29

Abdominal obesity, particularly excess intraperitoneal fat, is considered to play a major role in causing insulin resistance and NIDDM. To determine if NIDDM patients accumulate excess intraperitoneal fat, and whether this contributes significantly to their insulin resistance, 31 men with mild NIDDM with a wide range of adiposity were compared with 39 nondiabetic, control subjects for insulin sensitivity (measured using euglycemic-hyperinsulinemic clamp technique with [3-3H]glucose turnover) and total and regional adiposity (assessed by hydrodensitometry and by measuring subcutaneous abdominal, intraperitoneal, and retroperitoneal fat masses using magnetic resonance imaging [MRI], and truncal and peripheral skinfold thicknesses using calipers). MRI analysis revealed that intraperitoneal fat was not increased in NIDDM patients compared with control subjects; in both groups it averaged 11% of total body fat. NIDDM patients, however, had increased truncal-to-peripheral skinfolds thickness ratios. In NIDDM patients, as in control subjects, amounts of truncal subcutaneous fat showed a stronger correlation with glucose disposal rate than intraperitoneal or retroperitoneal fat; however, NIDDM patients were more insulin resistant at every level of total or regional adiposity. Further, no particular influence of excess intraperitoneal fat on hepatic insulin sensitivity was noted. We conclude that NIDDM patients do not have excess intraperitoneal fat, but that their fat distribution favors more truncal and less peripheral subcutaneous fat. Moreover, for each level of total and regional adiposity, NIDDM patients have a heightened state of insulin resistance.
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PMID:Relationship of generalized and regional adiposity to insulin sensitivity in men with NIDDM. 892 52

Obesity is a heterogeneous condition and not every obese patient is at increased risk of cardiovascular diseases (CVD). It is now well established that the regional distribution of body fat is a critical correlate of the metabolic complications of obesity. Studies that have assessed adipose tissue distribution by imaging techniques such as computed tomography have demonstrated the importance of the intra-abdominal (visceral) fat depot as a marker of a cluster of metabolic abnormalities which include glucose intolerance, insulin resistance, hyper-insulinemia, hypertriglyceridemia, elevated number of apo B-carrying lipoproteins as well as hypoalphalipoproteinemia. Although the association between visceral obesity and metabolic complications can hardly be questioned, it has been suggested that it may not necessarily represent a causal relationship. For instance, concomitant alterations in sex steroid levels have been found in both men and women with abdominal (visceral) obesity which have also been reported to be significantly correlated with the insulin resistant-dyslipidemic state found in abdominal obese subjects. In women, abdominal obesity is associated with increased free testosterone concentrations and reduced sex hormone binding globulin (SHBG) levels, whereas in men this condition is associated with reduced testosterone and adrenal C12 steroid (dehydroepiandrosterone, androstenedione, androstene-3 beta, 17 beta-diol) levels as well as decreased SHBG concentrations. These altered steroid and SHBG; levels have been reported to be independent correlates of the metabolic complications of visceral obesity although they cannot solely account for the increased CVD risk found in these patients. In this regard, intervention studies are clearly warranted to better quantity the respective contribution of excess visceral adipose tissue and of the concomitant alterations in sex steroid levels as modulators of metabolic disturbances increasing CVD risk in obesity.
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PMID:Obesity and metabolic complications: contribution of dehydroepiandrosterone and other steroid hormones. 894 99

Obesity, hypertension and hyperinsulinism are frequently related and constitute morbid elements of human athero-thrombogenic syndrom. To elucidate physiopathologic mechanisms linking these symptoms, we have developped an experimental model reproducing the morbid triptyque: obesity-hypertension-insulin resistance were induced by hyperlipidic hypercaloric diet. The aim of this study was to investigate cardiovascular modifications elicited by high fat diet. Four male Beagle-Harrier dogs were used in this preliminary study. We investigated before and 7 weeks after the beginning of the hypercaloric hyperlipidic diet morphologic measures, systemic blood pressure (BP) and heart rate (HR), pulmonary blood pressure, cardiac output (CO), systolic ejection volume (SEV), peripheral arterial resistance (PAR) and HR variability on 24 hours' electrocardiogram obtained by Holter method. Echocardiographic modifications of left ventricule was also studied after 20 weeks. Body weight increased (+15.4%) after 7 weeks and remained stable the whole experimental period. This gain was associated with an increase of thoracic and abdominal circonferences (respectively +5.9% and 14.3% at the 7th week). The abdominal increase was significantly more elevated than the thoracic one. This abdominal obesity was associated with an increase in diastolic (+17.9%) and mean (+16.4%) (but not systolic) BP. High fat diet failed to modify arterial pulmonary blood pressures but induced an increase in both CO (3.0 +/- 5.2 vs 4.3 +/- 0.4 ml/min) and SEV (32.4 +/- 5.2 vs 40.8 +/- 2.7 ml/beat). PAR decreased (43.1 +/- 5.9 vs 33.0 +/- 3.2 UW; p = 0.08). Holter method showed a non significant increase of HR (82.0 +/- 7.8 vs 99.5 +/- 5.6 beat/min; p = 0.1) explained by a significant decrease of parasympathetic HR variability (PNN50: 53.5 +/- 4.1 vs 40.9 +/- 4.1%). No echocardiographic modification of left ventricule was found after 20 weeks of high fat diet. This preliminary study shows that, like in humans, high fat diet in dogs induced abdominal obesity with systemic hypertension but failed to provoke left cardiovascular hypertrophy after 20 weeks. This model will allow to characterize the links between cardiovascular and endocrinometabolic alterations occurring during the development of obesity and hypertension.
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PMID:[Experimental hypertension induced by hypercaloric diet]. 894 71

Abdominal obesity has emerged as a strong and independent predictor for non-insulin dependent diabetes mellitus (NIDDM). Adiposity located centrally in the abdominal region, and particularly visceral as opposed to subcutaneous fat, is also distinctly associated with hyperlipidemia, compared with generalized distributions of body fat. These lipoprotein abnormalities are characterized by elevated very low density lipoprotein (VLDL) and low density lipoprotein (LDL) levels, small dense LDL with elevated apolipoprotein B levels, and decreased high density lipoprotein2b (HDL2b) levels. This is the same pattern seen in both familial combined hyperlipidemia and NIDDM. The pronounced hyperinsulinemia of upper-body obesity supports the overproduction of VLDL and the increased LDL turnover. We have proposed that an increase in the size of the visceral fat depot is a precursor to the increased lipolysis and elevated free fatty acid (FFA) flux and metabolism and to subsequent overexposure of hepatic and extrahepatic tissues to FFA, which then, in part, promotes aberrations in insulin actions and dynamics. The resultant changes in glucose/insulin homeostasis, lipoprotein metabolism, and vascular events then lead to metabolic morbidities such as glucose intolerance, NIDDM, dyslipidemia, and increased risk for coronary heart disease.
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PMID:Intra-abdominal fat: is it a major factor in developing diabetes and coronary artery disease? 896 90

We examined the association between psychosocial stress-related variables and insulin resistance syndrome (IRS) risk-factor clustering. In 90 middle-aged male volunteers, psychosocial stress-related variables, defined as feelings of excessive tiredness and as personality and behavioral factors reflecting a stress-inducing life-style (type A behavior, hostility, and anger), were significantly correlated with the hyperinsulinemia, hyperglycemia, dyslipidemia, hypertension, increased abdominal obesity, and increased plasminogen activator inhibitor-1 (PAI-1) antigen comprising the IRS. The correlations remained significant after adjusting for body mass index (BMI), age, educational level, smoking status, alcohol consumption, and physical activity. However, the different stress-related factors reflected different risk-factor clustering profiles. Type A behavior was associated with normotension and a normal metabolic profile (canonical r = .50, chi2(36) = 59.1, P = .008). Hostility was related to elevated systolic blood pressure (SBP) and elevated triglycerides (TGs) (canonical r = .38, chi2(14) = 23.2, P = .052), whereas feelings of excessive tiredness were related to abdominal obesity, augmented glycemic responses to glucose ingestion, dyslipidemia, and increased PAI-1 antigen (canonical r = .39, chi2(24) = 36.8, P = .046). Although hostility and feelings of excessive tiredness have partly overlapping but clearly different clinical and metabolic correlates, their combination represents a full-blown IRS. Thus, even though insulin resistance is presumably to some extent genetically determined, these results suggest that considering psychosocial stress may be beneficial in understanding IRS risk-factor clustering.
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PMID:Psychosocial stress and the insulin resistance syndrome. 896 88

The atherogenic profile of high triglyceride, reduced high-density lipoprotein (HDL) cholesterol, and small low-density lipoprotein particle size found in patients on chronic hemodialysis is known to be associated with insulin resistance and abdominal obesity in the general population. To assess the influence of insulin resistance and abdominal adiposity on the lipid profile in subjects on hemodialysis, intravenous glucose tolerance test and dual-energy x-ray absorptiometry were performed in 26 nondiabetic subjects on hemodialysis and compared with 22 nondiabetic control subjects matched for age, sex, and body mass index. Subjects on hemodialysis were found to have higher triglyceride (133 mg/dL [95% confidence interval, 115 to 159 mg/dL] v 97 mg/dL [95% confidence interval, 80 to 124 mg/dL]; P < 0.05), lower HDL cholesterol (36 +/- 3 mg/dL v 51 +/- 4 mg/dL [mean +/- SEM]; P < 0.01), enhanced insulin response to glucose (2.72 +/- 0.28 mUL(-1) min per mg dL(-1) v 1.67 +/- 0.22 mUL(-1) min per mg dL(-1); P < 0.01), and reduced sensitivity to the action of insulin (2.24 min(-1) per mUL(-1) min [95% confidence interval, 1.86 to 2.75 min(-1) per mUL(-1) min] v 4.17 min(-1) mUL(-1) min [95% confidence interval, 2.95 to 5.9 min(-1) per mUL(-1) min]; P < 0.01) than the control subjects. Abdominal adiposity measured by dual-energy x-ray absorptiometry (2,004 +/- 210 g v 2,163 +/- 198 g [mean +/- SEM]; P = NS) and percentage of body fat distributed to the abdomen (10.5% +/- 0.3% v 9.7% +/- 0.5% [mean +/- SEM]; P = NS) did not differ between the two groups. Subjects on hemodialysis were insulin resistant, but unlike control subjects, their lipid profile was not predicted by their insulin sensitivity. Abdominal adiposity was associated with a deteriorating lipid profile and insulin resistance in subjects on hemodialysis, as it was in control subjects. The presence of renal failure resulted in additional insulin resistance and a higher triglyceride level in the leaner subjects on hemodialysis compared with control subjects with similar levels of abdominal fat. In the more obese subjects, insulin sensitivity and triglyceride level did not differ between the two groups of subjects, although HDL cholesterol level remained low in subjects on hemodialysis. In conclusion, insulin resistance in subjects on hemodialysis did not directly account for their abnormal lipid profile. The negative impact of abdominal adiposity on the metabolic profile was preserved in subjects on hemodialysis, but the presence of renal failure itself resulted in insulin resistance in the leaner subjects and dyslipidemia in all subjects on hemodialysis compared with control subjects of comparable abdominal adiposity.
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PMID:The role of abdominal adiposity and insulin resistance in dyslipidemia of chronic renal failure. 900 30


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