Although each component of the metabolic syndrome can be targeted separately through pharmacotherapy, it is also possible to take a more global therapeutic approach to treating the metabolic syndrome and/or type 2 diabetes by focusing on reducing excess atherogenic/diabetogenic intra-abdominal adipose tissue, which is often present in patients with the clustering abnormalities of this syndrome. The causes of this preferential adipose tissue accumulation include an obesogenic and diabetogenic diet, a low level of physical activity leading to a positive energy balance, and genetic susceptibility. These causes should all be targeted to reduce the risk of developing the metabolic syndrome and type 2 diabetes (4). As depicted in Figure 1, abdominally obese individuals should be encouraged to increase their daily energy expenditure in order to decrease intra-abdominal adipose tissue and improve their plasma lipoprotein-lipid profile and indices of plasma glucose-insulin homeostasis. Typically, this loss of intra-abdominal adipose tissue reduces free fatty acid flux to the liver, which slows hepatic VLDL production, lowers plasma triglyceride and apolipoprotein B levels, and increases HDL cholesterol concentrations (5). It also changes the pattern of adipose tissue secretory products, causing interleukin-6 levels to fall and adiponectin concentrations to rise, which improves insulin sensitivity (6, 7). The end product of abdominal fat loss is a reduction in CRP levels.

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