Abstract
The pathophysiology of diabetic peripheral neuropathy (DPN) is multifactorial and both vascular factors with impairment of vasa nervorum and metabolic interactions are involved at all stages of DPN. The complex and interrelated effects of hyperglycemia include increased metabolic flux through the polyol pathway with consequent sorbitol and fructose accumulation, reduced myoinositol and sodium-potassium ATPase levels and altered protein kinase C activity.