Abstract
Postprandial state is a normal metabolic state throughout the day, due to the fact that the clearance of triglyceride- rich particles, preferably those of intestinal origin, continues for 6-8 hours after each daily meal. In 1979, Zilversmit postulated that atherosclerosis is a postprandial phenomenon. However, only recently the excessive and prolonged metabolic disturbances occurring in the postprandial state have regained interest as a potential cardiovascular risk factor. On the other hand, the molecular mechanisms by which postpandrial lipidaemia and the hyperglycaemia induce vascular damage have been recently described. These mechanisms include endothelial dysfunction, activation of adhesion molecules, activation of coagulation, oxidative stress and gene expression or genetic polymorphisms affecting genes involved in lipoprotein metabolism. Finally, we emphasize the importance of the composition of dietary fat, since it seems that a diet rich in monounsaturated fatty acids protects against the development of insulin resistance and decreases the incidence of type II diabetes mellitus.
Keywords: Postprandial lipidaemia, atherosclerosis, diet, genetic polymorphisms
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