Oxidative stress is present in the diabetic state. To determine whether STZ-diabetic nerves are susceptible to reperfusion, we evaluated the pathological consequences after 2.5 hours of ischemia followed by 3 and 24 hours of reperfusion in a 20-week STZ-diabetic rat sciatic nerve. Current perception threshold (CPT) at 250 Hz was employed to test the sensory function of three nerves: superficial peroneal, sural and posterior tibial. The “moving wall” represents the time period between the last issue available in JSTOR and the most recently published issue of a journal. Many times the diabetic will experience sores, cuts, and blisters on their feet that aren’t painful due to the nerves’ inability to transport the feeling of pain from the foot to the brain. These studies implicate disruption of normal hedgehog function in the etiology of diabetes-induced peripheral-nerve dysfunction and indicate that delivery of exogenous hedgehog proteins may have therapeutic potential for the treatment of diabetic neuropathy. Immunostaining shows depletion of NGF in keratinocytes in diabetic skin.
Some small fascicles had rates of axonal degeneration that far exceeded those of large adjacent fascicles. In diabetic nerves, tau(SD) is generally longer than normal, but hyperglycemia is associated with paradoxically shortened tau(SD), because of a decrease in axonal persistent Na+ conductance, possibly related to reduced membranous Na+ gradient, tissue acidosis, or other metabolic factors.