Diabetes, Vol 41, Issue 1 47-52, Copyright © 1992 by American Diabetes Association

ARTICLES

Effect of aminoguanidine on functional and structural abnormalities in peripheral nerve of STZ-induced diabetic rats

S Yagihashi, M Kamijo, M Baba, N Yagihashi and K Nagai
Department of Pathology and Neurology, Hirosaki University School of Medicine, Japan.

Nonenzymatic glycosylation of structural proteins and the formation of advanced glycosylation end products (AGEs) have been involved in the pathogenesis of diabetic complications. We examined the effect of aminoguanidine, a potent inhibitor of AGE formation, on functional and structural abnormalities in peripheral nerve of streptozocin-induced diabetic rats. Diabetic rats were treated with daily injections of 25 mg/kg body wt s.c. aminoguanidine (AG)-sulfate for 16 wk and compared to untreated diabetic rats. AG treatment improved motor nerve conduction velocity in 12- and 16-wk diabetic rats despite no changes in body weight, blood glucose, and HbAIc levels. AG treatment inhibited an accumulation of fluorescent AGE in diabetic nerves, and morphometric analysis of the sural nerve showed a partial effect on myelinated fiber size and axonal atrophy. These findings suggest that AG may have a beneficial effect on diabetic neuropathy and nonenzymatic glycosylation of peripheral nerve proteins.
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