Diabetic neuropathy is the one of the serious secondary complications of diabetes mellitus in which an alteration or a damage in nerve cells is observed. The nerve disorders can be developed at any time, but the possibility of the development increases with the longer duration of diabetes. The damage can be occurred in the sensory, motor, and autonomic nervous system, therefore the damage is observed in the innervated organs and systems. As a result, diabetic neuropathy is the most common cause of non-traumatic amputations and autonomic failure. In their lifetime, diabetic patients with diabetic neuropathy have a 15% incidence of undergoing one or more amputations. Due to the similarities of the presented pathologies to the human diseases and its the easiness, diabetes induced animal models are widely used in studies. Since diabetes and therefore diabetic neuropathy is a worldwide problem, it is necessary to examine the effects of diabetes mellitus on the neural system. The recorded compound action potentials revealed that diabetes is the reason of the significant increase in time to peak, rheobase and chronaxie values. Furthermore, the maximum depolarization, area, kinetics and the conduction velocities of both the fast and slow nerve fibers were found to be decreased. In addition to the decline of the conduction velocities, a shift from faster fibers to the slower ones was observed. Since the oxidant agents are unavoidable, the aim should be to minimize it as much as possible. For minimization, the antioxidant agents are crucial. It is also shown that beyond the inhibition of the oxidation agents, some of them also restore the damaged nerves. Currently to avoid diabetic neuropathy it is suggested to keep the glucose levels as close as possible to the normal values. If it is necessary pain therapy can be used to minimize the pain. The promising results of the animal studies show that the treatment strategies should be renewed by including the antioxidants to the daily diet to the diabetic patients.
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