Abstract:

Cardiovascular diseases are the most common causes of morbidity and mortality in diabetic patients. Oxidative stress plays an important role in diabetic endothelial dysfunction. Under conditions of oxidative stress, free oxygen radicals may increase insulin resistance and affect pancreatic beta cells. Several experimental animal models to understand the pathogenesis of diabetes mellitus have been developed, and the model including high fat diet which leads to insulin resistance is the best animal model to mimic type 2 diabetes mellitus. In diabetes mellitus, it is well known that there is an increase in lipid peroxidation. This condition is also associated with oxidative stress. Endothelial dysfunction creates imbalance between vasoconstriction and vasodilatation. In large arteries, nitric oxide plays a main role in endothelium-dependent vasodilatation. Abnormal production or response of nitric oxide contributes vascular and endothelial dysfunction in diabetes mellitus. Oxidative stress reduces the levels of nitric oxide and diminishes endotheliumdependent vasodilatation. Therefore, in recent years, the studies to treat the diabetic complications have focused on antioxidant agents. The goal of the treatment is to decrease oxidative stress, as well as lipid and glucose levels. Thus, endothelial dysfunction may be ameliorated and diabetic vascular complications can be avoided.

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