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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertensive obese subjects run an increased cardiovascular risk. Their predominantly abdominal obesity is often associated with hypertriglyceridaemia and insulin-resistant diabetes, and their cardiovascular status is characterized by cardiac hyperdynamics and hypervolaemia responsible for left ventricular hypertrophy and dilatation. Insulin resistance and subsequent hyperinsulinaemia are thought to explain the obesity-hypertension association, the cardiovascular effects observed and the metabolic and cardiovascular complications which might result from this situation. Successful control of both arterial pressure and overweight should contribute to regression of the left ventricular hypertrophy. Simultaneous treatment of abnormalities in carbohydrate and lipid metabolism is also necessary to prevent cardiovascular complications.
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PMID:[Cardiovascular consequences of obesity associated with arterial hypertension]. 146 76

Obesity has a multifactorial origin. However, although environmental variables undoubtedly play a role in the development of obesity, it is now clear that genetic variation is also involved in the determination of an individual's susceptibility to body fat accumulation. In addition, it is also widely accepted that obesity is not a single homogeneous phenotype. It is also heterogeneous regarding its causes and metabolic complications. The regional distribution of body fat appears to be an important correlate of the metabolic complications that have been related to obesity. Due to their higher accumulation of abdominal fat, men are generally more at risk for the metabolic complications of obesity than women whereas some obese women, with large gluteal-femoral adipose depots may have a cosmetic problem which may not necessarily require medical intervention. Several studies have been conducted to understand the mechanisms by which abdominal obesity is related to diabetes, hypertension and cardiovascular disease. It appears that the increased risk of abdominal obesity is the result of complex hormonal and metabolic interactions. Studies in genetic epidemiology have shown that both total body fatness and the regional distribution of body fat have a significant genetic component. Standardized intervention studies using an identical twin design have shown that individuals that have the same genetic background tend to show similar changes in body fat and in plasma lipoprotein levels when exposed to standardized caloric excess or energy restriction. Finally, although abdominal obesity is a significant risk factor for cardiovascular disease, not every abdominal obese subject will experience metabolic complications, suggesting that some obese individuals may be more susceptible than others. Variation in several genes relevant to lipid and lipoprotein metabolism may alter the relation of abdominal obesity to dyslipoproteinemias. Abdominal obesity should therefore be considered as a factor that exacerbates an individual's susceptibility to cardiovascular disease.
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PMID:Genetic aspects of susceptibility to obesity and related dyslipidemias. 151 6

All large prospective studies (n greater than 20,000) and several smaller studies have found that severe obesity [body mass index (BMI) greater than or equal to 35 kg/m2] is associated with approximately a twofold increase in total mortality and in a severalfold increase in mortality due to diabetes, cerebro-, and cardiovascular disease, and certain forms of cancer. Studies that have not been able to confirm this have been small and/or short term, have failed to control for smoking or early mortality, have controlled for intermediate risk factors in an inappropriate way, or have a reduced internal validity due to misclassification biases. As compared with BMI, abdominal obesity is a stronger predictor of mortality in most studies available. The incidence of sudden death unexplained by autopsy may be up to 40 times higher in severely obese subjects as compared with the general population. A small weight increase since the age of 18 is associated with a decreased risk whereas weight increases greater than 10 kg are associated with an increased mortality. The total mortality ratio for severe obesity decreases from 55 y of age and is not detectable above 80 y of age. Studies lacking adequate control groups indicate that a sustained weight loss may induce a reduced mortality but results from controlled intervention studies are so far not available.
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PMID:Mortality of severely obese subjects. 153 Oct 97

Insulin responses to intravenous glucose infusion and glucose utilization during hyperinsulinaemic euglycaemic clamp were determined in a large homogeneous group of 65-year-old male subjects. Twenty-eight had untreated Type 2 (non-insulin-dependent) diabetes mellitus and the remaining 44 control subjects had a normal glucose tolerance. Diabetic patients with abdominal obesity displayed peripheral insulin resistance in combination with defective insulin secretion, whereas non-obese diabetic patients showed only a secretory defect. Thus, Type 2 diabetes in obese and non-obese elderly male subjects may take two forms where the cause of hyperglycaemia differs.
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PMID:Different aetiologies of type 2 (non-insulin-dependent) diabetes mellitus in obese and non-obese subjects. 191 53

This review concentrates on recent prospective studies concerning evaluation of the health risk of obesity with special reference to the impact of the distribution of the adipose tissue. Analysis of the data indicates that adipose tissue localized to the abdominal region (especially intraabdominal fat) is associated with an enhanced risk profile including elevated levels of triglycerides and insulin, low levels of high density lipoprotein-cholesterol and elevated blood pressure. Abdominal obesity, determined by the waist/hip ratio, was associated with cardiovascular disease, premature death and non-insulin demanding diabetes mellitus. On the other hand, the total fat mass (measured as body mass index) was positively associated only with non-insulin demanding diabetes mellitus. The androgen/estrogen activity seems to be an important factor for determining the topographical localization of the adipose tissue. The great amount of free fatty acids which may be released from the abdominal fat tissue seemed to be of great pathogenetic importance for the metabolic consequences of abdominal obesity. In conclusion, obesity and the abdominal localization of adipose tissue seem to be two separate entities with different pathogenesis and clinical consequences. The abdominal obesity is the type which is predominantly associated with enhanced health risks. These associations may result in an altered strategy of treatment of the obese population.
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PMID:[Health risks of obesity. Significance of the regional distribution of adipose tissue]. 202 93

The health risks of obesity increase with its severity and reach significance at a weight greater than 20% above optimal, by using life insurance tables, or at a body mass index greater than 27. Risks include hypertension, insulin resistance and diabetes mellitus, cardiovascular disease, hypertriglyceridemia, low high-density-lipoprotein cholesterol, and, in some studies, high total-and low-density-lipoprotein cholesterol. There is an increased mortality from endometrial cancer in women and from colorectal cancer in men. Chronic hypoxia and hypercapnia, sleep apnea, gout, and degenerative joint disease can occur with more severe obesity. The distribution of body fat is directly related to these health risks. Abdominal obesity is more dangerous than gluteal-femoral obesity because the amount of intraabdominal fat seems to determine much of the increased peril; therefore, risks of cardiovascular disease, stroke, hypertension, and diabetes increase with abdominal obesity, even independently of total fat mass.
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PMID:Health implications of obesity. 203 92

Increased general and abdominal obesity has been independently associated with diabetes, increased risk of stroke, and coronary artery disease (CAD). It is more prevalent in developed countries and in urban areas of nonindustrialized nations than in less developed and rural areas. To evaluate the associations between general and abdominal obesity (as determined by total body fat, waist to hip ratio, umbilical to triceps ratio, and umbilical to subscapular ratio) with glucose, plasma lipoproteins, apolipoprotein (apo) A-I and B concentrations, and low density lipoprotein (LDL) particle size (LDL 1-7), we randomly selected 222 men and 243 women from rural and urban areas of Puriscal, Costa Rica. Abdominal obesity, as assessed by the waist to hip ratio, was independently and significantly associated with higher triglyceride levels (p less than 0.01) and with lower high density lipoprotein cholesterol levels (p less than 0.05) in men and women and with higher glucose levels (p less than 0.05) and smaller LDL particle size (p less than 0.01) in women. Abdominal obesity, as assessed by the umbilical to subscapular ratio, was independently and significantly associated with higher total cholesterol (p less than 0.005) and apo B (p less than 0.01) levels. Umbilical to triceps ratio was positively associated with blood pressure in men. Urban men had increased general and abdominal obesity (p less than 0.0001), number of cigarettes smoked per day (p less than 0.0001), and diastolic blood pressure (p less than 0.05) and had a decreased fitness level (p less than 0.0001) as well as higher (p less than 0.05) plasma glucose, triglyceride, and total cholesterol concentrations and lower (p less than 0.05) apo A-I and HDL cholesterol levels compared with rural men. The differences between rural and urban women were not as striking. Urban women had increased general and abdominal obesity, glucose, and apo B levels (p less than 0.05) and a decreased fitness level (p less than 0.0001). Our data indicate that general and abdominal obesity, increased cigarette smoking, diastolic blood pressure, and decreased fitness level are more prevalent in an urban than in a rural area in Costa Rica, particularly in men. The higher prevalence of such risk factors in the urban area is associated with a more atherogenic plasma lipoprotein profile.
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PMID:Relations of body habitus, fitness level, and cardiovascular risk factors including lipoproteins and apolipoproteins in a rural and urban Costa Rican population. 206 29

Elevated plasma levels of cholesterol and triglycerides, low levels of high-density lipoproteins, hypertension, diabetes mellitus, smoking and abdominal obesity are risk factors for coronary heart disease (CHD) and stroke. Because of the preventable threat to life, well-being and productivity from perturbations of plasma lipoproteins (which affect about 60% of adults), we recommend a population-based strategy with public education on diet, exercise and the hazards of smoking and legislation for better food labelling. This should be combined with the medical guidelines we describe to detect and treat those at highest risk for CHD (including about 15% of adults), who merit priority for the medical, dietetic and laboratory services required. Among people aged 40 years or more this includes those with plasma total cholesterol levels greater than 7 mmol/L, fasting triglyceride levels greater than 3 mmol/L or cholesterol level greater than 6 mmol/L when associated with CHD or other risk factors for CHD. For younger people the criteria for highest risk include cholesterol levels greater than 6.5 mmol/L for those aged 30 to 39 years, greater than 6 mmol/L for those aged 20 to 29 and greater than 5 mmol/L for those under age 20.
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PMID:Guidelines for the detection of high-risk lipoprotein profiles and the treatment of dyslipoproteinemias. Canadian Lipoprotein Conference Ad Hoc Committee on Guidelines for Dyslipoproteinemias. 263 69

It has been proposed that central obesity, by virtue of the enhanced lipolytic activity of abdominal adipose tissue, leads to higher plasma FFA concentrations, which, in turn, decrease both hepatic removal of insulin and insulin-stimulated glucose uptake by peripheral tissues. In short, the predicted consequences of abdominal obesity are elevations in circulating FFA and insulin levels as well as insulin resistance. The goal of this study was to evaluate the relationships predicted by the overall hypothesis; this study was carried out in 31 obese females, defined as having normal glucose tolerance (n = 12), impaired glucose tolerance (n = 8), or noninsulin-dependent diabetes mellitus (n = 11). Abdominal obesity was estimated by determining the ratio of waist to hip girth, fasting and postprandial plasma FFA and insulin concentrations were measured at hourly intervals from 0800-1600 h, and insulin-stimulated glucose disposal was quantified by the euglycemic hyperinsulinemic clamp technique. The first step in the postulated sequence of events to be tested was that the greater the WHR, the higher the total integrated plasma FFA response. The correlation coefficient between these two variables was 0.29, indicating that the results did not support the prediction. Furthermore, we could not demonstrate any relationship between the magnitude of the plasma FFA and insulin responses (r = 0.20; P = NS). However, there was a modest inverse relationship between height of circulating plasma insulin concentration and a decrease in insulin-stimulated glucose uptake (r = -0.43; P less than 0.03) in the group as a whole. On the other hand, when the three groups were analyzed individually, a significant inverse relationship was only seen in the control group (r = -0.67), and a direct relationship was actually seen in patients with impaired glucose tolerance (r = 0.88). Furthermore, when the mean responses for the variables in each of the three groups were compared, it was apparent that the postulated relationships between abdominal obesity, plasma FFA concentration, and insulin secretion and action were not present. Thus, the data presented do not support the hypothesis that differences in the degree of central obesity play an important role in regulation of plasma concentrations of either FFA or insulin or in modulation of insulin-stimulated glucose uptake in the patients we studied.
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PMID:Effect of central obesity on regulation of carbohydrate metabolism in obese patients with varying degrees of glucose tolerance. 222 87

The effects of free fatty acids (FFA) on insulin receptor binding and processing (internalization, degradation, dissociation, and release) were examined in hepatocytes isolated from 12-week-old female rats. Animals were fasted for 24 h to deplete liver glycogen and lipid content. Cells were preincubated for 30 min or 3 h at 37 degrees C in media containing 10 mM lactate, 1 mM pyruvate, and 3.5 percent albumin with increasing concentrations of palmitate (0.00, 0.05, 0.2, 0.5, 1.0 and 2.0 mM). Under these conditions palmitate is the primary substrate for cellular metabolism, and its major fate is oxidation. Equilibrium binding was determined after 18-20 h of incubation at 4 degrees C with radiolabeled insulin and increasing concentrations of unlabeled hormone. With increasing palmitate concentration, a dose-dependent decline in cell-surface insulin receptor binding was observed. Binding decreased by 35 percent and 44 percent after 30 min and 3 h of preincubation with 2 mM palmitate, respectively. This decrease was due to a reduction in insulin receptor number. Receptor-mediated insulin processing was evaluated in cells prelabeled at 4 degrees C with 125I (A14)-monoiodoinsulin at an insulin concentration of 100 pM and reincubated at 37 degrees C for up to 30 min. The amount of internalized insulin was decreased by preincubation of hepatocytes with palmitate. This decrease was proportional to the reduction in cell-surface insulin receptor density at palmitate concentrations of 0.05-0.5 mM, but was disproportionally greater at higher fatty acid concentrations. Receptor-mediated insulin degradation decreased at palmitate concentrations between 0.05 and 1.0 mM. At 2 mM, however, insulin degradation was enhanced. This enhancement was observed after 30 min or 3 h of exposure to the fatty acid. Dissociation and/or release of cell-associated internalized insulin was not influenced by the FFA exposure. The effects of FFA on hepatocyte insulin binding and processing were contingent upon cellular metabolism, since no changes were noted when cells were preincubated with palmitate at 4 degrees C under otherwise similar conditions. Thus the in vitro exposure of hepatocytes to FFA influences both receptor and postreceptor events mediating insulin metabolism. These effects may account for the altered hepatic insulin extraction and sensitivity that accompany abdominal obesity and its progression to diabetes.
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PMID:Receptor and postreceptor effects of free fatty acids (FFA) on hepatocyte insulin dynamics. 226 78


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