SLOWING OF PERIPHERAL MOTOR-NERVE CONDUCTION WAS AMELIORATED BY AMINOGUANIDINE IN STREPTOZOCIN-INDUCED DIABETIC RATS

The aims of this study were to investigate the effect of aminoguanidin e (AG) on slowing of motor nerve conduction velocity (MNCV) of the sci atic nerve in streptozocin-induced diabetic rats and to assess its mec hanism of action. The MNCV of the sciatic nerve was measured electroph ysiologically in diabetic rats treated with and without AG for 16 week s. To elucidate the action of AG, morphological lesion and abnormality of polyol pathway metabolism in the nerve were examined and tissue le vels of advanced glycosylation end-products (AGE) were determined as a n indicator of AGE accumulation in tissue. Diabetic rats were treated with AG at three doses of 10, 25 and 50 mg/kg for 16 weeks, Myelinated fiber morphometry and nerve Na+,K+-ATPase activity were determined. T he AGE levels in renal cortex were measured by a specific ELISA, Amino guanidine dose-dependently ameliorated slowing of MNCV 16 weeks after the treatment without changing body weight or blood glucose levels. No difference in myelinated fiber morphometry or Na+,K+-ATPase activity with or without AG treatment was detected in diabetic rats, Diabetes i ncreased the AGE level in the renal cortex by six times compared to no n-diabetic rats, and AG reduced the rise in the AGE level by 40%. The MNCV was inversely correlated with the AGE levels. We conclude that im provement of conduction slowing by AG in experimental diabetes may be through decreasing the AGE level in the peripheral tissues. Aminoguani dine may have a therapeutic potential in controlling diabetic peripher al neuropathy.