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Sorbitol, Myo-Inositol and Sodium-Potassium ATPase in Diabetic Peripheral Nerve

  • Section 1 The Polyol Pathway and Complications of Diabetes
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Summary

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.

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Greene, D.A. Sorbitol, Myo-Inositol and Sodium-Potassium ATPase in Diabetic Peripheral Nerve. Drugs 32 (Suppl 2), 6–14 (1986). https://doi.org/10.2165/00003495-198600322-00004

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