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 myo-inositol-related defect may contribute to other biochemical, functional and structural abnormalities of diabetic peripheral neuropathy.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003929:Diabetic Neuropathies / Q000378:metabolism* / Q000628:therapy; D004734:Energy Metabolism; D006801:Humans; D007294:Inositol / Q000378:metabolism* / Q000627:therapeutic use; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013012:Sorbitol / Q000378:metabolism*
D001786:Blood Glucose; D007294:Inositol; D013012:Sorbitol; D000254:Sodium-Potassium-Exchanging ATPase