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

Coronary heart disease (CHD) is the leading cause of death in women, and the risk of this disease rises markedly after loss of ovarian function. Hormone replacement therapy (HRT) can reduce the incidence of CHD in postmenopausal women by 50%. HRT causes changes in lipids and lipoproteins, but it is now clear that many other effects of gonadal steroid hormones have important influences on the cardiovascular system. These nonlipid effects include a variety of changes in other metabolic risk factors for CHD, as well as direct arterial effects. Insulin resistance and hyperinsulinaemia may be pivotal disturbances in the pathogenesis of CHD. Estradiol reverses the effects of menopause on glucose and insulin metabolism, resulting in an increase in pancreatic insulin secretion and a decrease in insulin resistance, although other types of estrogen may not do this. Androgenic progestogens may oppose this potentially beneficial effect on insulin resistance. Central obesity is linked with many CHD risk factors, and HRT reverses the increased fat distribution that results from loss of ovarian function at the menopause. HRT may also improve the balance between coagulation and fibrinolysis, resulting in a reduction in arterial thrombosis. Finally, estradiol acts directly on the arterial wall, modifying both endothelium-dependent and calcium-dependent processes. These actions result in improved blood flow and reduced blood pressure and, importantly, have the potential to reduce myocardial ischaemia.
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PMID:Hormone replacement therapy and the cardiovascular system. Nonlipid effects. 751 32

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

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

Unlike classical microvascular complications, large-vessel atherosclerosis can precede the development of diabetes, suggesting that rather than atherosclerosis being a complication of diabetes, both conditions have common genetic and environmental antecedents, i.e., they spring from a "common soil." It is now known that adverse environmental conditions, perhaps related to less-than-optimal nutrition, in fetal and early life are associated with an enhanced risk of both diabetes and cardiovascular disease many decades later. These same adverse environmental conditions are also associated with the development in adult life of abdominal obesity and the insulin-resistance syndrome (IRS). The IRS consists of glucose intolerance, hyperinsulinemia, dyslipidemia (high triglyceride and low high-density lipoprotein [HDL] cholesterol levels), and hypertension. Although the mechanism underlying this cluster is controversial, the statistical association is well established. All of the elements of the IRS have been documented as risk factors for type II diabetes. Some, but not all, of these elements are also cardiovascular disease risk factors, in particular, hypertension and low HDL cholesterol. Other factors associated with the IRS that may enhance cardiovascular disease risk are plasminogen activator inhibitor 1 and small, dense low-density lipoprotein particles. Whether insulin itself is a risk factor remains controversial, but recent epidemiological evidence has been mostly negative. This question has marked clinical relevance because if the IRS enhances cardiovascular disease risk by virtue of its concomitant factors and not the hyperinsulinemia per se, this would tend to alleviate concerns that intensive insulin management of type II diabetic subjects could enhance the risk of large-vessel atherosclerosis. Clinical trials are urgently needed to settle this point.
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PMID:Diabetes and cardiovascular disease. The "common soil" hypothesis. 769 2


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