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The exaggerated flux through polyol pathway during diabetes is thought to be a major cause of lesions in the peripheral nerves. Here, we used aldose reductase (AR)-deficient (AR^−/−) and AR inhibitor (ARI)-treated mice to further understand the in vivo role of polyol pathway in the pathogenesis of diabetic neuropathy. Under normal conditions, there were no obvious differences in the innervation patterns between wild-type AR (AR^+/+) and AR^−/− mice. Under short-term diabetic conditions, AR^−/− mice were protected from the reduction of motor and sensory nerve conduction velocities observed in diabetic AR^+/+ mice. Sorbitol levels in the sciatic nerves of diabetic AR^+/+ mice were increased significantly, whereas sorbitol levels in the diabetic AR^−/− mice were significantly lower than those in diabetic AR^+/+ mice. In addition, signs of oxidative stress, such as increased activation of c-Jun NH₂-terminal kinase (JNK …