Abstract
The role of sorbitol, myo-inositol, and Na +, K +-adenosine triphosphatase (ATPase) activity on motor nerve conduction velocity (MNCV) in streptozotocin (STZ)-diabetic rats was studied. Reduction of MNCV and Na +, K +-ATPase in caudal nerves appeared after 3 weeks of diabetes, and at this time treatment with aldose reductase inhibitor (ARI), ADN-138 and 1% myo-inositol supplement was begun. One percent myo-inositol supplement for 3 weeks resulted in a significant increase in myo-inositol levels in diabetic nerves, but left MNCV and sorbitol levels unchanged. In contrast, treatment with ADN-138 for 3 weeks reduced sorbitol levels in diabetic nerves and resulted in significant increases in MNCV and Na +,K +-ATPase in the nerves. Since ADN-138 did not restore myo-inositol levels, the increase in Na +, K +-ATPase levels by ADN-138 treatment was independent of myo-inositol levels. Also, nerve Na + levels in ADN-138-treated rats were reduced and the ratio of K + to Na + was raised, while 1% myo-inositol supplement did not affect them. These results suggest that treatment with ADN-138 elevates MNCV through a series of processes: ARI → reduction of sorbitol level → increase in Na +, K +-ATPase activity → correction of K +, Na + imbalance → increase in MNCV.
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