Abstract

There is increasing evidence that the post-prandial state is an important contributing factor to the development of atherosclerosis. In non-diabetic subjects the atherosclerotic risk factors comprised in the categories of lipids, coagulation system and endothelial function may be adversely modified in the post-prandial phase. The generation of an oxidative stress may be the common pathway through which eating may induce these alterations. In diabetic patients these phenomena may be amplified by post-prandial hyperglycemia.

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