Taurine reverses neurological and neurovascular deficits in Zucker diabetic fatty rats

F Li, OI Abatan, H Kim, D Burnett, D Larkin, IG Obrosova, Martin Stevens

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    61 Citations (Scopus)


    Increased oxidative stress is implicated in the pathogenesis of diabetic peripheral neuropathy (DPN). However, the efficacy of antioxidant therapy on DPN complicating type 2 diabetes remains unexplored. We therefore determined the ability of the antioxidant taurine to reverse deficits of hind limb sciatic motor and digital sensory nerve conduction velocity (NCV), nerve blood flow (NBF), and sensory thresholds in hyperglycemic Zucker diabetic fatty (ZDF) rats. Experimental groups comprised lean nondiabetic (ND), ND treated with taurine (ND + T), untreated ZDF diabetic (D), and D rats treated with taurine (D + T). Compared to ND rats, 23%, 15% and 56% deficits of motor NCV, sensory NCV and NBF, respectively as well as thermal and mechanical hyperalgesia were reversed by taurine. An 84% deficit of dorsal root ganglion neuron calcitonin gene-related peptide in D rats was prevented by taurine. In summary, the antioxidant taurine reverses neurological and neurovascular deficits in experimental type 2 diabetes.
    Original languageEnglish
    Pages (from-to)669-
    JournalNeurobiology of Disease
    Publication statusPublished - 1 Jun 2006


    • taurine
    • neuropathy
    • calcitonin
    • antioxidant
    • gene-related peptide
    • type 2 diabetes


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