Publication: Contribution of the serine kinase c-Jun N-terminal kinase (JNK) to oxidant-induced insulin resistance in isolated rat skeletal muscle
Issued Date
2012-12-01
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ISSN
17444160
13813455
13813455
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2-s2.0-84869420795
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Mahidol University
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SCOPUS
Bibliographic Citation
Archives of Physiology and Biochemistry. Vol.118, No.5 (2012), 231-236
Suggested Citation
Fernando R. Santos, Maggie K. Diamond-Stanic, Mujalin Prasannarong, Erik J. Henriksen Contribution of the serine kinase c-Jun N-terminal kinase (JNK) to oxidant-induced insulin resistance in isolated rat skeletal muscle. Archives of Physiology and Biochemistry. Vol.118, No.5 (2012), 231-236. doi:10.3109/13813455.2012.713366 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/13556
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Title
Contribution of the serine kinase c-Jun N-terminal kinase (JNK) to oxidant-induced insulin resistance in isolated rat skeletal muscle
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Abstract
The specific and direct contribution of the stress-activated serine kinase c-Jun N-terminal kinase (JNK) in the development of oxidative stress-induced insulin resistance of the glucose transport system in mammalian skeletal muscle is not fully understood. We assessed the specific role of JNK in the development of insulin resistance caused by in vitro exposure of rat soleus muscle to low levels (30-40 μM) of the oxidant hydrogen peroxide (H2O2) for up to 6h. Oxidant exposure caused significant (p < 0.05) decreases in insulin-stimulated glucose transport activity (up to 42%) and Akt Ser 473 phosphorylation (up to 67%), and increased (up to 74%) phosphorylation (Thr 183 /Tyr 185 ) of JNK1 and JNK2/3 isoforms. Importantly, insulin-stimulated glucose transport activity in the presence of H2O2 was moderately improved with the selective JNK inhibitor SP600125. These results indicate that activation of the serine kinase JNK contributes, at least in part, to oxidative stress-induced insulin resistance in isolated mammalian skeletal muscle. © 2012 Informa UK, Ltd.