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In this issue, Miyauchi and colleagues (1) present a study in which they have administered aminoguanidine orally for 16 weeks to young rats with streptozotocininduced diabetes. Whereas motor nerve conduction velocity (MNCV) kept increasing with time in the nondiabetic control rats and reached a plateau at 16 weeks, initially no such increase was noted in diabetic rats on aminoguanidine. However, after 2 months of treatment a dose-dependent progressive increase in MNCV was noted, which, at the dose of 50 mg/kg body weight, reached almost normal levels at 16 weeks. Morphometric analysis of the sciatic nerve revealed no significant differences between diabetic animals receiving aminoguanidine and controls. The improvement in MNCV did not appear to relate to glycemic status or amelioration in body weight, both of which were unchanged at 16 weeks compared to what they were at study onset. Somewhat surprising is the fact that Na+, K+-ATPase activity in
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