REDUCED MOTOR-NERVE CONDUCTION-VELOCITY AND NA-K+-ATPASE ACTIVITY IN RATS MAINTAINED ON L-FUCOSE DIET - REVERSAL BY MYOINOSITOL SUPPLEMENTATION()

L-Fucose is a monosaccharide that occurs in low concentrations in norm al serum but has been shown to be increased in diabetic individuals. I n cultured mammalian cells, L-fucose is a potent competitive inhibitor of myo-inositol transport. Abnormal myo-inositol metabolism has been proposed to be a factor in the development of diabetic complications. To test the hypothesis that myo-inositol deficiency may be responsible for the electrophysiological and biological defects in diabetic neuro pathy, rats were fed a diet containing 10 or 20% L-fucose for a period of 6 wk. After 3 wk, the L-fucose diets in two groups of rats were su pplemented with 1% myo-inositol. At the end of the study protocol, mot or nerve conduction velocity, sciatic nerve tissue Na+-K+-ATPase activ ity, and myo-inositol content were determined. These results were comp ared with those of STZ-induced diabetic rats fed either a normal diet or a diet containing 1% myo-inositol or with those given 450 mg/kg bod y wt of sorbinil. SeruM L-fucose levels were significantly increased i n rats fed a diet containing 10 or 20% L-fucose. In comparison, the se rum L-fucose levels in the diabetic rats were increased to a lesser ex tent. Motor nerve conduction velocity was significantly slower in rats fed a 10 or 20% L-fucose diet. Sciatic nerve composite and ouabain-se nsitive Na+-K+-ATPase activity and myo-inositol content was also signi ficantly decreased. Supplementation of 1% myo-inositol to the L-fucose -containing diet restored nerve myo-inositol levels and significantly improved Na+-K+-ATPase activity and motor nerve conduction velocity. I n diabetic rats, similar changes were prevented by treatment with myo- inositol or sorbinil. These observations suggest that myo-inositol def iciency may be a major factor in the development of neural defects ass ociated with acute diabetic neuropathy.