Diabetic peripheral neuropathy is the most common latě complication of diabetes mellitus which frequently results in clinically significant morbidities e.g. pain, sensory deficits, foot ulcers and amputations. During its natural course it progresses from initial functional to latě poorly reversible structural changes. Various interconnected pathogenetic concepts of diabetic neuropathy based on metabolic and vascular factors mostly derived from long-term hyperglycemia háve been proposed. These pathogenetic mechanisms háve been targeted in several experimental and clinical trials which, for example. tested restoration of normoglycemia by pancreas or islet transplantation, polyol pathway blockade by aldose reductase inhibitors, mitigation of oxidative stress and correction of abnormalities in essential fatty acid metabolism or of growth factor deficits. Unfortunately, so far no treatment based on pathogenic considerations has been introduced into clinical practice and thus optimal glycemic control aimed at preventing the occurrence of Írreversible structural nerve changes should be instituted immediately at the time of diagnosis of diabetes.

        Key words: diabetic neuropathy; pathogenesis; experimental and clinical studies of therapy.