Abstract:
:Accumulative evidence has supported the role of nitric oxide (NO) in a variety of normal physiological functions as well as many pathological conditions. In this study, we examined the possible diabetogenicity of NO by measuring the expression of the insulin receptor substrate (IRS)-1 in rat hepatocytes and skeletal myocytes. IRS-1 is important in the insulin-mediated signal transduction pathway in both liver and skeletal muscle. Exogenous NO donated by S-nitroso-N-acetylpenicillamine (SNAP) and S-nitrosoglutathione (GSNO) resulted in significant reduction in levels of IRS-1 in both cells, when compared to the insulin-stimulated control (p<0.001). Reversal to near normal levels was achieved using the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (carboxy-PTIO). SNAP was the more potent drug, and the skeletal myocytes were the more sensitive cells to the inhibitory effects of NO released from the drugs. These results provide further evidence that exogenous NO is a potent modulator of insulin-mediated signal transduction and may play a significant role in the pathogenesis of type 2 diabetes mellitus.
journal_name
J Biomed Scijournal_title
Journal of biomedical scienceauthors
Badal S,Brown PD,Ragoobirsingh Ddoi
10.1007/s11373-006-9073-ykeywords:
subject
Has Abstractpub_date
2006-07-01 00:00:00pages
561-8issue
4eissn
1021-7770issn
1423-0127journal_volume
13pub_type
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journal_title:Journal of biomedical science
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pub_type: 杂志文章,评审
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journal_title:Journal of biomedical science
pub_type: 杂志文章
doi:10.1186/1423-0127-19-86
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journal_title:Journal of biomedical science
pub_type: 杂志文章,评审
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journal_title:Journal of biomedical science
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journal_title:Journal of biomedical science
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journal_title:Journal of biomedical science
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journal_title:Journal of biomedical science
pub_type: 杂志文章
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journal_title:Journal of biomedical science
pub_type: 杂志文章,评审
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