Experimental diabetic neuropathy: an update

Diabetic neuropathy consists of several clinical syndromes affecting motor, sensory and autonomic nerves. Of these the most common is distal symmetric sensory polyneuropathy usuary referred to as diabetic neuropathy. Animal s tudies, mainly in diabetic rodents, have contributed tremendously to our un derstanding of this disease. From these it is clear that the pathogenesis o f diabetic neuropathy is multifactorial involving sequentially occurring an d often closely interrelated metabolic aberrations. Major pathogenetic mech anisms include increased activity of the polyol pathway, abnormalities in v asoactive substances, non-enzymatic glycation, increased presence of free r adicals, and perturbed neurotrophism. Traditionally the neuropathies accomp anying Type I (insulin-dependent) and Type II (non-insulin-dependent) diabe tes mellitus have been regarded as identical. Recent investigations have, h owever, clearly delineated distinct differences in the functional and struc tural expressions of the neuropathies in the two types of diabetes. Major f uture challenges are the identification of the differences in underlying pa thogenetic mechanisms in the two types of neuropathy and in gaining a bette r understanding of the hierarchy of the multifactorial mechanisms underlyin g the disease. This will be important for designing meaningful therapies wh ich to date have failed miserably in diabetic neuropathy.