Obesity, especially visceral obesity, is associated with a cluster of metabolic complications increasing the risk of type 2 diabetes and CHD. It has been shown that obese patients characterized by a high accumulation of visceral adipose tissue have increased glycemic and insulinemic responses to an oral glucose loan compared to normal weight individuals or to obese individual with a low accumulation of visceral adipose tissue. Viscerally obese patients are also characterized by an unfavourable plasme lipid profile which includes elevated triglyceride and apolipoprotein B concentrations, reduced HDL-cholesterol level as well as in increased poroportion of small, dense LDL Such changesin the lipid profile are often observed even in the absence of elevated LDL-cholesterol. Metabolic triad of non-traditional risk factors (hyperinsulinemia, elevated apolipoprotein B levels, increased proportion of small, dense LDL particels) was associated with a 20-fold increase in lthe risk of CHD. Indeed, less than 10% of men with a waist circumference below 90 cm and triglyceride concentrations below 2 mmol/l were characterized by the features of the metabolic triad. However, more than 80% of individuals with a waist circumderence above 90 cm and triglyceride levels above 2 mmol/l were carriers of the metabolic triad. Finally, an elevated visceral adipose tissue accumulation has also been associated with a thrombogenic and a pro-inflammatory metabolic profile which would be predictive of an unstable atherosclerotic plaque. Therefore, the stabilisation of the atherosclerotic plaque may represent a legitimate therapeutic objective to reduce the risk of CHD among patients with visceral obesity. It is recommended that a rather modest weight loss (approximately 10%) could contribute to substantially improve the risk profile of these patients.
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