Abstract

Peripheral neuropathy is a major late complication of diabetes mellitus. The pathogenesis is multifactorial. Changes in polyol pathway flux, oxidative stress, non-enzymatic protein glycation, endothelial dysfunction leading to reduced nerve blood flow, disturbed calcium homeostasis and deficits in neurotrophic factors probably all contribute to the clinical and neurophysiological findings in the diabetic patient with neuropathy. The present review focuses on animal models that are currently used to evaluate these pathophysiological mechanisms, and on the possibility of therapeutic pharmacological intervention. © 1997 John Wiley & Sons, Ltd.

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