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

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

Insulin secretion, clearance dynamics, and their relationship to peripheral plasma insulin and glucose levels were monitored during three 12-h periods of overnight rest, intake of three meals, and continuous enteral feeding of mixed nutrients. The low-frequency ultradian and the high-frequency insulin secretion pulsatility characteristics during the steady-states of overnight rest and continuous enteral feeding were also examined. In abdominally obese subjects, the insulin secretion rate was consistently higher than normal by 2.3-fold. Peripheral plasma insulin levels were increased by 3.4-fold during the overnight period and by 4- to 5-fold during the two fed states. Endogenous insulin clearance was significantly reduced during feeding. Both low- and high-frequency insulin secretory pulsatilities were detected in the abdominally obese subjects. Pulse periods were within the normal range. Pulse maxima, nadirs, and absolute amplitudes were increased concomitant with the increase in insulin secretion. Ultradian relative pulse amplitudes, however, were blunted. A significantly higher pulse-to-pulse variability was observed in the abdominally obese subjects compared with normal subjects. Furthermore, a significantly higher level of interindividual variability in the nutrient-stimulated insulin secretion and in the ultradian pulse characteristics was observed. Thus in abdominal obesity, the increase in pancreatic insulin output is limited and the secretory pulsatilities are aberrant, suggesting a defect in the insulin secretory process. Diminished insulin clearance contributes to the degree of peripheral hyperinsulinemia compensating for the insulin resistance characteristic of this form of obesity.
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PMID:Splanchnic insulin dynamics and secretion pulsatilities in abdominal obesity. 831 21

The purpose of this study was to examine the relationship of body mass index, abdomen-hip ratio, and dietary intake to fasting and postprandial insulin concentrations among 652 men aged 43-85 y, followed in the Normative Aging Study. Log-transformed fasting insulin was significantly associated with body mass index, abdomen-hip ratio, total fat energy, and saturated fatty acid energy, with correlation coefficients ranging from 0.14 for total fat to 0.45 for body mass index. When multivariate models were used, body mass index, abdomen-hip ratio, and saturated fatty acid intake were statistically significant independent predictors of both fasting and postprandial insulin concentrations, after age, cigarette smoking, and physical activity were adjusted for. If saturated fatty acids as a percentage of total energy were to decrease from 14% to 8%, there would be an 18% decrease in fasting insulin and a 25% decrease in postprandial insulin. These data suggest that overall adiposity, abdominal obesity, and a diet high in saturated fatty acids are independent predictors for both fasting and postprandial insulin concentrations.
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PMID:Relationship of dietary saturated fatty acids and body habitus to serum insulin concentrations: the Normative Aging Study. 833 37

The cardiovascular risk factor plasminogen activator inhibitor type 1 (PAI-1) has been associated with abdominal obesity, hypertension, hypertriglyceridemia, hyperinsulinemia, glucose intolerance, and type II diabetes, conditions known to be linked with insulin resistance. To determine whether PAI-1 is related to insulin resistance, we studied nine obese nondiabetics and 10 obese type II diabetics by means of a sequential hyperinsulinemic euglycemic clamp study. Plasma PAI-1 antigen (Ag) correlated significantly with peripheral insulin resistance, represented by the insulin level at which peripheral glucose uptake (PGU) is half-maximal ([ED50PGU] r = .87, P < .001). Multiple regression analysis including indices of hepatic and peripheral insulin action, fasting plasma insulin levels, triglyceride levels, blood pressure (BP), waist to hip ratio (WHR), and body mass index (BMI) disclosed ED50PGU to account for 76% of the variance of PAI-1 Ag. We suggest that PAI-1 contributes to the increased cardiovascular risk encountered with insulin resistance.
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PMID:The cardiovascular risk factor plasminogen activator inhibitor type 1 is related to insulin resistance. 834 17

Obesity can result in alterations in cardiac structure and function even in the absence of systemic hypertension and underlying organic heart disease. Increased total blood volume creates a high cardiac output state that may cause ventricular dilatation and ultimately eccentric hypertrophy of the left (and possibly the right) ventricle. Eccentric left ventricular (LV) hypertrophy produces diastolic dysfunction. Systolic dysfunction may ensue due to excessive wall stress if wall thickening fails to keep pace with dilatation. This disorder is referred to as obesity cardiomyopathy. The presence of systemic hypertension in obese individuals facilitates development of LV dilatation and hypertrophy. Congestive heart failure may occur in such individuals, and may be attributable to LV diastolic dysfunction or to combined LV diastolic and systolic dysfunction. The sleep apnea/obesity hypoventilation syndrome occurs in 5% of morbidly obese individuals and is potentially life-threatening. Treatment of obesity cardiomyopathy consists of weight loss, salt restriction, and diuretics. Digitalis and vasodilators may be useful in selected cases. Central obesity is probably a risk factor for the development of coronary heart disease. Alterations in lipid and insulin metabolism may facilitate development of coronary heart disease in obese patients.
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PMID:Obesity and the heart. 836 92

Diabetes is more common in Aborigines than in other Australian populations, even in groups that have lived in contact with Europids for 150 years. Prevalence data on hyperinsulinaemia and obesity from urbanized south eastern Australian Aborigines are presented with Europid comparisons. Aborigines had higher mean insulin levels than Europids. In females, mean fasting insulin was 15.5 mU/l in Aborigines, compared with 9.5 mU/l in Europids (P < 0.001). The means for males were 15.1 mU/l (Aborigines) and 8.3 (Europids) (P < 0.005). Obesity was more prevalent in Aborigines. In Aboriginal females aged 25-64 years, 41/108 (38%) had BMI > 30.0, compared with 37/208 (18%) Europids (P < 0.001). In males, the difference in the prevalence of obesity in Aborigines (17/69, 25%) and Europids (34/195, 17%) was not statistically significant. Waist-hip ratio was significantly greater among Aboriginal females (mean 0.87 in persons aged 25-64 years) than among Europids (mean 0.81, P < 0.001). In males, the mean ratio in Aborigines and Europids was the same (0.94). Abdominal obesity was most prevalent among Aboriginal females. For females aged 20-49 years, 83/110 (75%) Aborigines had a waist-hip ratio > 0.80, compared with 71/165 (43%) Europids (P < 0.001). Being overweight or obese is perceived with least accuracy by Aboriginal males of the four ethnicity/gender groups. Comparisons with national data suggest a gradient in the prevalence of obesity, lowest in urban groups, more in the country, and higher still among Aborigines, which is in reciprocal order to socio-economic status. In multivariate analyses, the association of BMI with insulin was highly significant. Hyperinsulinaemia in an Aboriginal group after many years of contact with Europids may result from environmental as well as genetic influences. Relative hyperinsulinaemia is not found among those Aborigines who have developed glucose intolerance, which could be explained by earlier pancreatic exhaustion in this group.
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PMID:Hyperinsulinaemia and obesity in aborigines of south-eastern Australia, with comparisons from rural and urban Europid populations. 837 69

The effects of female sex hormones on insulin binding and receptor-mediated insulin degradation were investigated in hepatocytes from ovariectomized rats. The influences of perinatal and peripubertal androgenization on these events were examined. Estradiol treatment increased insulin binding and receptor-mediated insulin degradation by increasing cell surface insulin receptor number. Progesterone also increased both binding and degradation, but the increase in degradation exceeded the increase in binding. Perinatal exposure to testosterone blunted the estradiol-induced increase in insulin binding and decreased degradation, whereas the progesterone-mediated increases were completely suppressed. Peripubertal testosterone decreased binding, with a much greater reduction in insulin degradation. Perinatal androgenization did not influence the peripubertal testosterone effects. Thus peripubertal female sex hormones exert regulatory influences on both hepatic cell surface insulin receptor number and postreceptor events mediating insulin degradation. These events are modulated by perinatal and peripubertal exposure to androgens. Abnormalities in sex hormone levels and/or hepatic androgenization could therefore contribute to altered insulin metabolism and hyperinsulinemia in some hyperandrogenized women with abdominal obesity and increased androgenic activity.
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PMID:Female sex hormones, perinatal, and peripubertal androgenization on hepatocyte insulin dynamics in rats. 846 Jun 82

A mother and her daughter with a novel type of familial partial lipodystrophy were studied. Both had atrophy of fat in the face, chest, and upper and lower limbs and abdominal obesity caused by intraabdominal fat accumulation. The mother had severe insulin resistance and impaired glucose tolerance, whereas the daughter had normal glucose tolerance and normal insulin sensitivity. Both had metabolic rates about 30% above normal levels, but normal thyroid function and plasma lipids.
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PMID:An unusual type of familial lipodystrophy. 853 May 81

Recent evidence suggests that non-insulin-dependent diabetes mellitus (NIDDM) and cardiovascular disease, rather than being related as underlying disease and complication, share common genetic and environmental antecedents, that is, they "spring from the same soil." Fetal and early-life nutritional deficiencies appear to predispose persons to both NIDDM and cardiovascular disease in later life. The insulin resistance syndrome, including abdominal obesity, may constitute the intermediate link between fetal and early-life nutritional deficiency and later disease. The insulin resistance syndrome includes insulin resistance, hyperinsulinemia, abdominal obesity, dyslipidemia with high triglyceride and low high-density lipoprotein cholesterol levels, and hypertension. Each element of the insulin resistance syndrome has been firmly established as a risk factor for development of diabetes. In addition, most of these elements are also well-recognized cardiovascular risk factors, although the weight of evidence now suggests that hyperinsulinemia itself is not. This last point is significant because of concern that aggressive insulinization of diabetic patients, which has been proved to reduce microvascular complications, might paradoxically increase the risk for large-vessel atherosclerosis. Available clinical trials suggest that this fear is unwarranted, but definitive trials are needed to resolve this important clinical question.
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PMID:Do non-insulin-dependent diabetes mellitus and cardiovascular disease share common antecedents? 855 1

Contrary to the popular belief, coronary heart disease (CHD) is indeed common in the Indian sub-continent. Expatriate Indians in their newly adopted countries have 3 to 5 times more chance of developing CHD than the native population or the other immigrant groups. The well-known risk factors such as hypercholesterolemia, hypertension and smoking do not appear to play a major role, while the syndrome of insulin resistance seems to be an important risk factor for CHD in people of this sub-continent. Abdominal obesity, hypertriglyceridemia, and low plasma HDL cholesterol are the markers of this syndrome. Increased plasma insulin levels or even better, the C-peptide measurement may help in identifying the abnormality early. As CHD among Indians has been found to be severe and more diffuse with serious complications and increased mortality at a younger age, preventive measures need to be instituted early. Low fat and complex carbohydrate diet along with regular aerobic exercise may help reduce abdominal obesity, improve insulin sensitivity and HDL cholesterol levels. Hypertriglyceridemia uncontrolled by above measures may require pharmacotherapy with agents such as gemfibrozil. Smoking must be stopped to help reduce insulin resistance and improve HDL levels and endothelial function. Those with hypertension should be considered for therapy with ACE inhibitors, which may improve insulin sensitivity. In patients with insulin resistance, therapy with metformin or troglitazone may be helpful.
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PMID:Special features of coronary heart disease in people of the Indian sub-continent. 855 88


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