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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Only limited effects of aminoguanidine treatment on peripheral nerve function, (Na+,K+)-ATPase activity and thrombomodulin expression in streptozotocin-induced diabetic rats.

AIMS/HYPOTHESIS: Aminoguanidine, a potent anti-glycation reagent, is known to be beneficial in experimental diabetic neuropathy. In this study, we explored the mechanisms of how aminoguanidine inhibits neuropathic changes in diabetes and compared its effects with those of insulin treatment. METHODS: Wistar rats, aged 8 weeks, were made diabetic by streptozotocin and given aminoguanidine dissolved in drinking water (1 g/l) for 8 weeks. Effects of daily insulin (protamine-zinc) treatment were also examined for comparison. At the end of the 8 weeks, we examined the peripheral nerve function and (Na+,K+)-ATPase activity and their relation to serum thrombomodulin concentrations that are considered as a marker of endothelial injury. RESULTS: Aminoguanidine treatment reduced the diabetes-induced decrease in tibial nerve conduction velocity by 47% (p < 0.05 vs untreated diabetic rats) and inhibited the loss of sciatic nerve (Na+,K+)-ATPase activity by 54% (p < 0.05 vs untreated diabetic rats). Insulin-treatment of diabetic rats restored these variables by 83% and 75%, respectively (both, p < 0.01 vs untreated diabetic rats). Thrombomodulin concentrations were increased (p < 0.01) in diabetic rats compared with those in non-diabetic controls and unaffected by aminoguanidine treatment. In contrast, the concentrations remained within the normal range in the insulin-treated group. CONCLUSION/INTERPRETATION: Although aminoguanidine treatment improved nerve conduction velocity and (Na+,K+)-ATPase activity, its effects were considerably less than those of insulin and were not apparent in some measures of endothelial cell injury.[1]


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