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

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

The amount of abdominal visceral adipose tissue measured by computed tomography is a critical correlate of the potentially "atherogenic" metabolic disturbances associated with abdominal obesity. In this study conducted in samples of 81 men and 70 women, data are presented on the anthropometric correlates of abdominal visceral adipose tissue accumulation and related cardiovascular disease risk factors (triglyceride and high-density lipoprotein cholesterol levels, fasting and postglucose insulin and glucose levels). Results indicate that the waist circumference and the abdominal sagittal diameter are better correlates of abdominal visceral adipose tissue accumulation than the commonly used waist-to-hip ratio (WHR). In women, the waist circumference and the abdominal sagittal diameter also appeared more closely related to the metabolic variables than the WHR. When the samples were divided into quintiles of waist circumference, WHR or abdominal sagittal diameter, it was noted that increasing values of waist circumference and abdominal sagittal diameter were more consistently associated with increases in fasting and postglucose insulin levels than increasing values of WHR, especially in women. These findings suggest that the waist circumference or the abdominal sagittal diameter, rather than the WHR, should be used as indexes of abdominal visceral adipose tissue deposition and in the assessment of cardiovascular risk. It is suggested from these data that waist circumference values above approximately 100 cm, or abdominal sagittal diameter values > 25 cm are most likely to be associated with potentially "atherogenic" metabolic disturbances.
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PMID:Waist circumference and abdominal sagittal diameter: best simple anthropometric indexes of abdominal visceral adipose tissue accumulation and related cardiovascular risk in men and women. 814 Oct 87

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

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 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

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

Although resistance to insulin-mediated glucose disposal has emerged as a link between abdominal obesity and hypertension, abnormalities of nonesterified fatty acid metabolism may play a greater role. Analyses were performed on existing data from 17 abdominally obese subjects (11 hypertensive, 6 normotensive) to determine whether fatty acid concentration and turnover were related to blood pressure independently of hyperinsulinemia and resistance to insulin-mediated glucose disposal. Glucose utilization, fatty acid concentration, and fatty acid turnover were obtained fasting and during euglycemic hyperinsulinemia at 10 and 40 mU/m/min. Analyses were also performed on another group of 30 subjects with a wide range of risk factors who had blood pressure data as well as glucose and fatty acid measurements during an insulin tolerance test. Fatty acid concentration and turnover were markedly more resistant to suppression by insulin in obese hypertensive than in lean or obese normotensive individuals. In the 17 obese subjects, blood pressure measured at screening, in the laboratory, and over a period of 24 hours correlated significantly with fatty acid concentration and turnover but not with glucose disposal measured during the hyperinsulinemic clamp. These correlations remained significant after fasting insulin, the insulin area under the curve during an oral glucose tolerance test, and glucose disposal during the clamp were controlled for. In the second group of subjects, plasma fatty acids 15 minutes after intravenous insulin also correlated with blood pressure. These correlations remained significant after insulin and an index of sensitivity to insulin-mediated glucose disposal were statistically controlled for. The data indicate that blood pressure is related to the effects of insulin on fatty acid metabolism. The findings raise the possibility that resistance of hormone-sensitive lipase to insulin participates in elevating the blood pressure of abdominally obese hypertensive subjects by increasing fatty acid concentration and turnover.
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PMID:Obesity hypertension is related more to insulin's fatty acid than glucose action. 861 31

The effects of testosterone treatment of abdominally obese men have been assessed by evaluating the following parameters: The metabolic activity of different adipose tissue regions in vivo (using lipid label as a tracer) and in vitro (measuring lipoprotein lipase (LPL) activity), the total and visceral adipose tissue mass, insulin sensitivity, fasting blood glucose, blood lipids, and blood pressure as well as prostate volume. Middle-aged men with abdominal obesity were treated with transdermal administration of testosterone (T), dihydrotestosterone (DHT) or placebo (P) during 9 months. The study was double-blind. Treatment with T was followed by an inhibited uptake of lipid label in adipose tissue triglycerides, a decreased LPL-activity and an increased turn-over rate of lipid label in the abdominal adipose tissue region in comparisons with the DHT and P groups. These effects on adipose tissue metabolism were not detected in the femoral adipose tissue region in any of the groups. T treatment was also followed by a specific decrease of visceral fat mass (measured by CT-scan), by increased insulin sensitivity (measured with the euglycemic glucose clamp), by a decrease in fasting blood glucose, plasma cholesterol and triglycerides as well as a decrease in diastolic blood pressure. In the DHT group an increased visceral mass was detected. No other changes in these variables were found in the DHT and P groups. There were no detectable changes in prostate volume (measured by ultra-sound), prostate specific antigen concentration, genito-urinary history or urinary flow measurements in any of the groups. It is suggested that T substitution to a selected group of men results in general metabolic and circulatory improvements. The prostate area needs further careful attention.
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PMID:Testosterone and regional fat distribution. 869 64

The prevalence of diabetes mellitus and impaired glucose tolerance (IGT) and their relationship to age and obesity was estimated in the rural town of Shikarpur in Sindh Province, Pakistan by a population-based survey in 1994. Oral glucose tolerance tests were performed in a stratified random sample of 967 adults (387 men, 580 women) aged 25 years and above. The diagnoses of diabetes and IGT were made on the basis of WHO criteria. The response rate was 71% for men and 80% for women. The prevalence of diabetes was 16.2% (9.0% known, 7.2% newly diagnosed) in men, and 11.7% (6.3% known, 5.3% newly diagnosed) in women. The prevalence rose with age to a peak of 30% and 21% in 65-74 year-old men and women respectively. IGT was detected in 8.2% of men and 14.3% of women. Thus, total glucose intolerance (diabetes and IGT combined) was present in 25% of subjects examined. These results indicate that glucose intolerance in South Asians can no longer be regarded as a problem confined to migrant communities. Of the 72 subjects previously known to have diabetes, none was using insulin treatment, but 57 (79%) took oral hypoglycaemic agents. Central obesity and positive family history were strongly associated with diabetes, as was prevalence of hypertension. The association with central obesity was greater for women than for men, and suggests important, modifiable risk factor(s) related to lifestyle.
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PMID:Pakistan national diabetes survey: prevalence of glucose intolerance and associated factors in Shikarpur, Sindh Province. 875 Feb 23

Excessive deposition of visceral adipose tissue is known to predispose to cardiovascular diseases. Considerable epidemiological and experimental evidence suggests that many physiological factors are involved in the aetiology of premature atherosclerosis associated with visceral obesity. Insulin resistance is frequently associated with abdominal obesity, and probably plays an important role in the pathophysiology of hypertriglyceridaemia, low levels of plasma high-density lipoprotein (HDL)-cholesterol, hypertension and reduced fibrinolytic activity. Exercise training may counteract the aberrant metabolic profile associated with abdominal obesity both directly and as a consequence of body fat loss. Exercise may increase insulin sensitivity, favourably alter the plasma lipoprotein profile and improve fibrinolytic activity. Changes in the activity of insulin-sensitive glucose transporters and of skeletal muscle lipoprotein lipase are some of the possible explanations for the increased insulin sensitivity and improved blood lipid profile associated with regular exercise. This review presents physical training as a relevant nonpharmacological tool in the treatment of abdominal obesity and associated metabolic disorders. The impact of regular exercise on the different aspects of the insulin resistance syndrome is discussed. The roles of gender, age and the state of insulin resistance on the metabolic effect of physical training are also considered.
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PMID:Effects of exercise training on abdominal obesity and related metabolic complications. 877 9


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