Vascular disease is the primary cause of morbidity and mortality in diabetics. Diabetic vascular disease is disseminated and includes renal capillary hypertrophy, reduced wound repair, impaired angiogenesis, and rapid and excessive hyperplasia after endovascular intervention [1, 2]. No single biochemical aberration unifies the diffuse nature of diabetic vascular disease. Hyperglycemia has been implicated, and yet glucose effects persist long after restoration of euglycemia. It is possible that acute fluctuations in glucose concentration have prolonged cell and tissue effects.

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