Prevention of platelet dysfunction by vitamin E in diabetic atherosclerosis.

Premature atherosclerosis and other vascular disorders are serious complications of diabetes mellitus. Contributing factors include (i) increased peroxidation of LDL leading to foam cell formation, fatty streaks and plaque formation in the arterial wall, and (ii) hyperreactivity of blood platelets leading to increased platelet adhesion and aggregation. Vitamin E may play a protective role as an antioxidant and/or membrane stabilizing agent in either mechanism. In platelets it appears to regulate arachidonic acid metabolism. Decreased vitamin E levels in platelets are associated with increased aggregation. This is reversible by correction of the vitamin E status. In diabetics, platelet vitamin E levels tend to be reduced with concomitant increase in platelet aggregation. Several studies in patients with insulin-dependent diabetes mellitus and, to some extent, in those with non-insulin-dependent diabetes mellitus have shown that supplementation with several hundred IU vitamin E significantly reduced platelet aggregation and lipid peroxidation. In healthy volunteers high-dose supplementation had no notable effect on platelet aggregation. However, doses as low as 200 IU vitamin E significantly reduced platelet adhesion and inhibited the formation of protruding pseudopods typically occurring in activated platelets. In diabetic patients a decrease in the nonenzymatic glycation of proteins by vitamin E supplementation has been observed. Controlled studies are needed to confirm the effect of vitamin E on platelet function in well-defined groups of diabetics, followed by large-scale trials investigating the prevention of diabetic vascular complications as clinical end point.