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Prevention of platelet dysfunction by vitamin E in diabetic atherosclerosis

Schutzwirkung von Vitamin E auf Plättchenfunktion in der Atherogenese bei Diabetikern

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Summary

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.

Zusammenfassung

Diabetes mellitus ist durch verfrühte Atherosklerose und andere vaskuläre Komplikationen gekennzeichnet. Zu den auslösenden Faktoren gehören 1. erhöhte Peroxidation von LDL, was zu Schaumzellbildung und Plaques in der Arterienwand führt, und 2. Hyperreaktivität von Blutplättchen mit erhöhter Adhäsions- und Aggregationsneigung. Vitamin E könnte in seiner Funktion als Antioxidans oder Membranstabilisator eine Schutzwirkung ausüben. In Plättchen ist es an der Regulierung des Arachidonsäuremetabolismus beteiligt.

Bei erniedrigten Vitamin-E-Konzentrationen in Plättchen ist die Aggregation erhöht. Dies wird durch Korrektur des Vitamin-E-Status normalisiert. Bei Diabetikern besteht eine Tendenz zu reduzierten Vitamin-E-Werten mit gleichzeitig gesteigerter Plättchenaggregation. Mehrere Studien in Patienten mit Insulin-abhängigem und zum Teil mit nicht-Insulin-abhängigem Diabetes mellitus haben gezeigt, daß durch die Gabe einiger hundert IU Vitamin E die Aggregation sowie die Lipidperoxidation reduziert werden können. In gesunden Kontrollen konnte keine Wirkung auf die Aggregation festgestellt werden, hingegen führten Dosen von nur 200 IU Vitamin E zu einer signifikanten Reduktion der Adhäsion, wobei die Ausstülpungen von Pseudopoden, wie sie für aktivierte Plättchen typisch sind, nicht gebildet wurden. Bei Diabetikern führte die Gabe von Vitamin E auch zu einer Verminderung der nicht-enzymatischen Glykation von Proteinen.

Diese präliminären Befunde müssen durch randomisierte und kontrollierte Studien in gut definierten Patientengruppen ergänzt werden, um die Wirkung von Vitamin E auf die Plättchenfunktion zu erhärten.

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Gerster, H. Prevention of platelet dysfunction by vitamin E in diabetic atherosclerosis. Z Ernährungswiss 32, 243–261 (1993). https://doi.org/10.1007/BF01611163

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