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dc.contributor.authorRoglio, Ilaria-
dc.contributor.authorBianchi, R.-
dc.contributor.authorGiatti, S.-
dc.contributor.authorCavaletti, G.-
dc.contributor.authorCaruso, D.-
dc.contributor.authorScurati, Samuele-
dc.contributor.authorCrippa, D.-
dc.contributor.authorGarcía-Segura, Luis M.-
dc.contributor.authorCamozzi, F.-
dc.contributor.authorLauria, G.-
dc.contributor.authorMelcangi, R. C.-
dc.identifierdoi: 10.1007/s00018-007-7002-5-
dc.identifierissn: 1420-682X-
dc.identifier.citationCellular and Molecular Life Sciences 64: 1158-1168 (2007)-
dc.description.abstractIn this study we have assessed the effect of testosterone (T), dihydrotestosterone (DHT) and 5αandrostan-3α, 17β-diol (3α-diol) therapies on diabetic neuropathy. Diabetes was induced in adult male rats by the injection of streptozotocin and resulted in decreased T and increased 3α-diol levels in plasma and in decreased levels of pregnenolone and DHT in the sciatic nerve. Moreover, a reduced expression of the enzyme converting Tinto DHT (i.e., the 5α-reductase) also occurs at the level of sciatic nerve, suggesting that the decrease of DHT levels could be due to an impairment of this enzyme. Chronic treatment for 1 month with DHT or 3α-diol increased tail nerve conduction velocity and partially counteracted the increase of thermal threshold induced by diabetes. Treatment with DHT increased tibial Na+,K+-ATPase activity and the expression of myelin protein P0 in the sciatic nerve.DHT, 3α-diol and T reversed the reduction of intra-epidermal nerve fiber density induced by diabetes. These observations indicate that T metabolites can reverse behavioral, neurophysiological, morphological and biochemical alterations induced by peripheral diabetic neuropathy. © 2007 Birkhäuser Verlag.-
dc.publisherBirkhäuser Verlag-
dc.titleTestosterone derivatives are neuroprotective agents in experimental diabetic neuropathy-
dc.description.versionPeer Reviewed-
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