Abstract
Type 2 diabetes (T2D) is a major cause of vascular complications affecting heart, kidney, retina and peripheral nerves. Hyperglycaemia leads to oxidative stress that plays an important role in vascular degenerative lesions observed in diabetes. In this Review we consider whether vitamin E, zinc or selenium are involved in the pathogenesis of diabetes. Concerning vitamin E, major epidemiological studies do not give the expected results in preventing cardiovascular outcomes. The mechanisms of free radical overproduction in diabetes could explain these results. Superoxide anion overproduction originates from mitochondria; in these conditions antioxidant enzymes are more relevant to reduce oxygen species than vitamin E. Zinc has numerous targets to modulate insulin activity, including its antioxidant capacity. Zinc status is decreased in most T2D patients. The effect of zinc supplementation on antioxidant status is raised when complications are associated. Selenium is a major antioxidant trace element and is the co-factor of glutathione peroxidase (Se GSHpx). Low Se GSHpx activity, observed in diabetic patients, is associated with thrombosis and cardiovascular complications.
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