ABSTRACT
Clinical studies in both type 1 and 2 diabetes indicate that chronic hyperglycemia is implicated in the pathogenesis of both somatic and autonomic diabetic neuropathy (1–6). The Diabetes Control and Complications Trial (DCCT) showed that improved glycemic control can reduce the rate of both somatic and autonomic neuropathy in type 1 diabetes (7, 8), while similar effects are observed in type 2 diabetes (9). Recent interest has focused on the association between early impaired glucose regulation (impaired glucose tolerance [IGT] and impaired fasting glucose [IFG]) and diabetic microvascular and macrovascular complications. However, even optimal glycemic control cannot completely prevent the development of neuropathy, so alternative forms of therapy are required. Recent evidence implicates induction of reactive-oxygen species (ROS) in neuronal cytotoxicity, both in vitro and in vivo (10–14).
