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

Abdominal obesity increases the estrogen-to-androgen ratio and may increase sympathetic nervous activity, both hypothesized to influence the development of benign prostatic hyperplasia and the severity of urinary obstructive symptoms. In 1986 and 1987, men aged 40-75 years who were participants in the Health Professionals Follow-up Study and who were without prior diagnosis of cancer or prostatectomy provided data on weight, height, and waist and hip circumferences. The men were followed for incidence of prostatectomy for benign prostatic hyperplasia up to January 1992. In addition, the frequency and severity of symptoms of urinary obstruction were assessed among respondents to a questionnaire in 1992. Among 25,892 men who provided complete information for both surgery and symptoms, 837 men had surgery for benign prostatic hyperplasia, and 2,581 of those without surgery reported frequent urinary symptoms. After adjustment for age, smoking, and body mass index, abdominal obesity was related to prostatectomy (odds ratio (OR) = 2.38, 95% confidence interval (CI) 1.42-3.99, for those with a waist circumference > or = 43 inches (109 cm) relative to those with a waist circumference < 35 inches (89 cm); p trend < 0.0001) and with frequent urinary symptoms among those without prostatectomy (OR = 2.00, 95% CI 1.47-2.72; p < 0.0001). Body mass index, hip circumference, and waist-to-hip ratio were not associated with benign prostatic hyperplasia independently of waist circumference. These results suggest that abdominal obesity in men may increase the frequency and severity of urinary obstructive symptoms and may increase the likelihood that such obese men will undergo a prostatectomy.
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PMID:Obesity and benign prostatic hyperplasia. 752 82

Recent research has indicated that visceral obesity is associated with multiple endocrine disturbances. Insulin resistance, as well as visceral fat accumulation, may be consequences of these abnormalities. The complex endocrine aberrations are probably of central origin, and suggest a neuroendocrine background with a "hypothalamic arousal" syndrome. Such a syndrome has been found after excess alcohol intake, tobacco smoking, and certain types of stress reactions. Subjects with visceral obesity might be characterized by a high prevalence of such factors, although only indirect evidence is available for the stress component, maybe caused by a poor socioeconomic and psychosocial situation. In primate experiments, a submissive stress reaction is followed by a syndrome essentially identical to that seen in humans with visceral obesity, including visceral fat accumulation. These observations strongly support a similar chain of events in humans. Recent studies have indicated several abnormalities in cerebrospinal fluid (CSF) concentrations of catecholamines and neuropeptides. In particular, serotonin metabolites and corticotropin-releasing factor (CRF) concentrations are apparently lower than normal. In women with visceral obesity, these low concentrations are associated with food choices that indicate a preference for carbohydrates. This finding emphasizes the importance of serotonin agonists in the treatment of human obesity. It seems possible that such drugs may have effects on metabolic and other symptoms particularly prevalent in abdominal obesity, and that these effects might be independent of the decrease in energy intake. It would seem highly desirable to explore these possibilities further. Such observations may also provide a link between the abnormalities of low serotonin and CRF concentrations in the central nervous system on one hand and peripheral metabolic and other abnormalities on the other.
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PMID:Neuroendocrine abnormalities in human obesity. 753 80

Considerable evidence indicates that obesity, and in particular abdominal obesity, is a risk factor for both heart disease and non-insulin dependent diabetes mellitus. In spite of this, little is known of the regulation of triacylglycerol synthesis in adipose tissue other than by insulin. Acylation stimulating protein (ASP), a human plasma protein, stimulates triacylglycerol synthesis in adipose tissue and is also produced by human adipocytes. ASP may play a physiological role in the regulation of efficiency of adipose tissue fat storage and affect clearance of triglycerides from plasma.
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PMID:The acylation stimulating protein-adipsin system. 755 May 36

Obesity is usually defined on the basis of body composition measurements. Body composition can be assessed using elaborate methods or anthropometry. Obese children are characterized by increased serum total cholesterol and triglycerides, reduced high-density-lipoprotein(HDL)-cholesterol concentrations, and hyperinsulinemia. Such a metabolic profile may create favorable conditions for atherogenesis and cardiovascular disease later in life. In fourty obese children aged 6-14 years were evaluated plasma insulin after OGTT, serum lipids and body composition. The correlation analysis between insulin, lipids and fat mass (%), based on skinfold measurements was not significative. These results are possible because with skinfold measurements are not separated the subcutaneous and intraabdominal compartments; infarct, only abdominal obesity is associated with the increased risk factors (hyperinsulinemia, hyperlipidemia, ecc.).
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PMID:[The lipid status, insulinemia and fat mass in 40 children with essential obesity]. 756 42

To determine whether the combination of obesity and hypertension results in additive defects in oxidative and nonoxidative glucose metabolism and the association of these changes with altered hemodynamic actions of insulin, we studied 11 abdominally obese hypertensive, 6 abdominally obese normotensive, and 7 lean normotensive nondiabetic subjects. Endogenous glucose production and glucose metabolized were calculated from a euglycemic clamp at 72 and 287 pmol insulin/m2 per minute. Glucose metabolized divided by insulin was lower at 72 pmol/m2 per minute in both obese groups than in lean normotensive subjects, at 148 +/- 14, 144 +/- 33, and 373 +/- 69 (mumol/m2 per minute)/(pmol/L), respectively (P < .01). Similar results were obtained during the higher insulin dose. Nonoxidative and oxidative glucose disposals by indirect calorimetry were lower in both abdominally obese groups (P < .05). Hepatic glucose production was completely suppressed in lean subjects at the lower insulin dose and in all three groups at the higher insulin dose. Hemodynamic responses during the clamp were not significantly different among the three groups. Abdominal obesity is associated with defects in insulin-regulated oxidative and nonoxidative glucose disposal as well as in insulin suppression of hepatic glucose production. Mild hypertension does not exacerbate these defects. Whereas the global impairment in glucose metabolism suggests the presence of an early defect or defects, including reduced tissue perfusion, systemic and regional hemodynamic responses to insulin were not altered. These findings do not support a direct role for insulin resistance in the pathogenesis of the hypertension associated with abdominal obesity.
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PMID:Glucose metabolism in abdominally obese hypertensive and normotensive subjects. 760 22

The purpose of this study was to examine the effects of a total body strength-training program on changes in total and regional body composition, in particular intra-abdominal adipose tissue (IAAT), in older women. Fourteen healthy older women (mean age 67 +/- 1 yr) exercised 3 times/wk for 16 wk. Strength was assessed by one-repetition maximum tests, with training intensity gradually increased to approximately 67% of one repetition maximum. Body composition was measured by hydrodensitometry and regional body composition was measured by computed tomography. Strength was significantly increased in the upper (51%) and lower body (65%). There was no significant change in body weight (64.4 +/- 2.7 vs. 64.2 +/- 2.7 kg), total body fat (38.7 +/- 1.4 vs. 38.0 +/- 1.6%) or fat-free mass (39.7 +/- 1.0 vs. 40.0 +/- 0.9 kg). However, after ST, there were significant reductions in IAAT (143.9 +/- 13.3 vs. 130.0 +/- 12.4 cm2), the IAAT-to-subcutaneous adipose tissue ratio (0.48 +/- 0.04 vs. 0.44 +/- 0.04), and midthigh subcutaneous adipose tissue (141.7 +/- 11.5 vs. 133.6 +/- 10.8 cm2) and an increase in midthigh muscle (52.9 +/- 2.6 vs. 58.0 +/- 2.0 cm2) (all P < 0.05). In conclusion, significant reductions in IAAT and an increase in strength and muscle area were observed after a strength-training program in healthy older women. These changes may be important in preventing the negative health outcomes associated with the age-related increase in intra-abdominal obesity.
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PMID:Reduction in intra-abdominal adipose tissue after strength training in older women. 761 51

Numerous studies show increasing evidences that a low post-prandial triglyceride metabolic capacity is likely to favour cardio-vascular disease, particularly coronary and cerebro-vascular atherosclerosis. Because of high fasting triglycerides, low HDL and high LDL3 lipid profile, abdominal obesity and insulin-resistance, Type 2 diabetic patients are candidates to altered post-prandial lipemia. However many practical and methodological difficulties remain concerning the nature, lipid quantity and composition of the lipid load, the choice of accurate markers of liver derived lipoproteins, pointing out the urgent need for a standardization procedure.
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PMID:[Post-prandial lipemia in diabetes. How? Why?]. 762 70

The susceptibility of LDL to copper-catalyzed oxidation was evaluated in 24 patients with insulin-dependent and 16 patients with non-insulin-dependent diabetes mellitus, 14 abdominal and 14 gluteal-femoral obese women, 22 familial hypertriglyceridemic and 28 control subjects. Differences in the LDL susceptibilities were studied by measuring the changes of fluorescence intensity and expressed as lag-phase. The lag-phase was significantly shorter in patients with insulin-dependent, non-insulin-dependent diabetes mellitus, abdominal obesity and familial hypertriglyceridemic patients than in gluteal-femoral obese subjects and controls (p < 0.01). The shortest lag-phase was found in familial hypertriglyceridemic patients while intermediate values were found in insulin-dependent, non-insulin-dependent and abdominal obese patients who had only a slight increase in triglyceride values. Similarly the lowest value of the LDL cholesterol to protein ratio, as expression of LDL particle size, was found in familial hypertriglyceridemic patients (p < 0.01), while the patients with insulin-dependent, non-insulin-dependent diabetes mellitus and abdominal obesity had intermediate values. The ratio was found to be directly correlated with the length of the lag-phase (r = 0.87, p < 0.001). In spite of similar triglyceride and cholesterol to protein ratio values, however, the length of the lag-phase was significantly shorter in patients with insulin-dependent diabetes mellitus than in those with abdominal obesity. So it is concluded that the different susceptibility to oxidation found in the different groups of patients is only partially explained by plasma triglyceride values.
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PMID:Increased susceptibility of LDL to in vitro oxidation in patients with insulin-dependent and non-insulin-dependent diabetes mellitus. 764 91

Experimental data as well as logical considerations suggest that the increased cardiovascular risk associated with abdominal obesity is mediated primarily by increased levels and flux of free fatty acids. Practical strategies for decreasing free fatty acid levels and/or flux may include: a very-low-fat, low-glycemic-index diet; promotion of insulin sensitivity (via exercise training, chromium, soluble fiber or drugs); anti-lipolytic agents; and stimulation of hepatic lipid oxidation with hydroxycitrate, carnitine and possibly fish omega-3s. Fortunately, many of these measures should also promote a leaner physique. Thus, even when abdominal obesity cannot be corrected, it may prove feasible to mitigate its dangers.
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PMID:Reduction of free fatty acids may ameliorate risk factors associated with abdominal obesity. 766 29

Central obesity in association with insulin resistance is a strong predictor of coronary artery disease (CAD) in South Asians; however the prevalence of central obesity and insulin resistance in Indians are unknown. Anthropometric measurements, dietary intakes, physical activity and prevalence of risk factors and CAD were obtained in 152 adults between 26-65 years of age (80 males, 72 females) selected by random sampling from urban population of Moradabad. The overall prevalence of central obesity was 539 per 1000 adults including 56.2% in males and 51.3% in females. The prevalence of glucose intolerance, diabetes mellitus, hypertension, hypertriglyceridemia and CAD were significantly higher in the higher quintiles of WHR above 0.88 compared to lower quintiles. Fasting and postprandial glucose, plasma insulin and triglycerides as well s total cholesterol and blood pressure were significantly higher in each of the upper quintile of WHR with increase in WHR compared to lowest quintile of WHR below 0.81. These findings indicate the existence of a modest degree of insulin resistance with a modest tendency to central obesity in the urban population of North India. The prevalence of CAD was significantly (p < 0.01) higher among subjects with central obesity than in non-obese subjects (21.5 vs 3.2%). Underlying these findings, the prevalence of central obesity was significantly greater among sedentary and mild activity group compared to moderate and heavy activity group and per day energy expenditure during activity in the upper quintiles with WHR > 0.88 was significantly less compared to energy expenditure in lower quintiles of WHR. Similarly dietary fat intake in the upper quintiles of WHR was also significantly higher than in the lower quintiles of WHR. These findings suggest that populations with higher prevalence of central obesity and CAD may be benefited with an aim to decrease central obesity.
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PMID:Epidemiologic study of central obesity, insulin resistance and associated disturbances in the urban population of North India. 767 61


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