Triglyceride‐rich lipoproteins in non‐insulin‐dependent diabetes mellitus: post‐prandial metabolism and relation to premature atherosclerosis

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Abstract
Non‐insulin‐dependent diabetes mellitus is frequently associated with premature atherosclerosis. Abnormalities in lipid and lipoprotein metabolism contribute to the increased risk of coronary heart disease. One of the most common lipid abnormalities in non‐insulin‐dependent diabetes mellitus is hypertriglyceridaemia. In the present paper, the authors review the metabolism of triglyceride‐rich lipoproteins, with special emphasis on the post‐prandial state. Several studies have demonstrated that levels of atherogenic post‐prandial lipoproteins are increased in patients with non‐insulin‐dependent diabetes mellitus. An increased supply of glucose and free fatty acids contributes to overproduction of very low‐density lipoproteins, increasing the burden of triglyceride‐rich lipoproteins on the common lipolytic pathway at the level of lipoprotein lipase. Low lipoprotein lipase activity and increased amounts of lipolysis‐inhibiting free fatty acids further impair lipolysis of post‐prandial lipoproteins. The clearance of atherogenic remnants is also delayed in non‐insulin‐dependent diabetes mellitus. There is evidence that a relative hepatic removal defect exists, secondary to impaired remnant‐receptor interaction and increased competition with very low density lipoprotein remnants. Correction of the increased post‐prandial lipaemia in non‐insulin‐dependent diabetes mellitus is advisable, as it may contribute to attenuation of the risk on premature atherosclerosis. When dietary measures and hypoglycaemic agents have failed to achieve acceptable lipid levels, lipid‐lowering drugs should be advised. Fibric acids and hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitors are the drugs of choice.