Obesity, an extremely prevalent health problem in our society, is associated with increased risk of atherosclerosis and its complications. When seen mostly in the abdominal region, obesity tends to associate with a lipoprotein pattern of elevated triglycerides, milder elevations of LDL-cholesterol, and lowered HDL-cholesterol levels. The mechanism by which this pattern occurs is complex, and likely involves increased fatty acid delivery to the liver, causing increased production of triglyceride-rich lipoproteins. This greater utilization of fatty acid substrates and reduced utilization of carbohydrate substrates may produce a state of relative hyperglycemia and the resulting hyperinsulinemia may further contribute to hepatic triglyceride production. Increased lipolysis of triglyceride-rich particles is also seen in obese subjects, thus representing an overall increase in the metabolic activity of adipose tissue in obese subjects. Lowering of HDL-cholesterol likely reflects the increased lipolysis of triglyceride-rich particles. Weight loss, if gradual and sustained, is associated with reversal of these lipoprotein abnormalities, independent of alterations in dietary fat intake. A combination of diet and exercise seems to have the greatest long-term benefit, with significant improvements seen even without normalization of weight.
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