Pathogenesis of Diabetic Neuropathy

Abstract

Diabetic peripheral neuropathy (DPN), which is characterized by nerve fiber atrophy and loss (1), is a multifactorial disorder resulting from complex interrelated metabolic and vascular defects. It is common, frequently underdiagnosed, and has been reported to be present in 39% of healthy insulin-dependent diabetic patients (in the Diabetes Control and Complications Trial [DCCT]) (2) and may afflict over 50% of diabetic subjects after 25 yr of diabetes (3) or 44% of diabetic subjects between 70–79 yr of age (4). Although the DCCT has definitively implicated hyperglycemia in its pathogenesis and progression (2,5), the resulting defects in glucose metabolism underlying diabetic neuropathy remain to be identified, and their interaction with other elements in the diabetic milieu (e.g., deficiencies of insulin and other growth-factors, oxidative stress, and so on) remain uncertain. Moreover, the precise cellular localization of the deficits remains highly speculative (6–8). Keywords Nitric Oxide Nerve Growth Factor ATPase Activity Diabetic Neuropathy Aldose Reductase These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.