Sorbitol, Myo-Inositol and Sodium-Potassium ATPase in Diabetic Peripheral Nerve
Slowing of nerve conduction, a hallmark of both experimental and human diabetic neuropathy, is improved or corrected by aldose reductase inhibitors such as sorbinil Animal experiments suggest that a myo-inositol-related defect in nerve sodium-potassium adenosine triphosphatase (ATPase) is responsible for the acute reversible slowing of nerve conduction in diabetes mellitus. This myo-inositol-related defect is at present viewed as a cyclic metabolic defect. Aldose reductase inhibitors have been shown to restore to normal both the myo-inositol content and the sodium-potassium ATPase activity of nerve. This suggests that the acute effects of aldose-reductase inhibitors on nerve conduction in both diabetic animals and human patients may be modified by the correction of an underlying myo-inositol-related defect of nerve sodium-potassium ATPase. Furthermore, this myoinositol-related defect may contribute to other biochemical, functional and structural abnormalities of diabetic peripheral neuropathy.
KeywordsNerve Conduction Diabetic Neuropathy Aldose Reductase Diabetic Peripheral Neuropathy Sorbinil
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