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/IRS-1 and Akt and insulin resistance in muscle of mice
1 Internal Medicine, Universidade Estadual de Campinas, UNICAMP, Campinas, Brazil
* To whom correspondence should be addressed. E-mail: msaad{at}fcm.unicamp.br.
We have previously demonstrated that the insulin resistance associated with iNOS induction in two different models of obesity, diet induced obesity and the ob/ob mice, is mediated by S-nitrosation of proteins involved in insulin signal transduction: insulin receptor 
subunit (IR), insulin receptor substrate 1(IRS-1) and Akt. S-nitrosation of IRProcessing report for the following articles:
In this study, we observed that LPS induced insulin resistance in the muscle of wild type mice, as demonstrated by reduced insulin-induced tyrosine phosphorylation of IR and IRS-1, reduced IRS-1 expression and reduced insulin-induced serine-phosphorylation of Akt. This resistance occurred in parallel with enhanced iNOS expression, which was accompanied by S-nitrosation of IR/ IRS-1 and Akt.
In the muscle of iNOS|-/- mice, we did not observe enhanced iNOS expression, nor any S-nitrosation of IR|/ IRS-1 and Akt after LPS treatment. Moreover, insulin resistance was not present. The preservation of insulin-induced tyrosine-phosphorylation of IR and IRS-1, of IRS-1 protein expression and of insulin-induced serine-phosphorylation of Akt, observed in LPS treated iNOS-/- mice strongly suggests that the insulin resistance induced by LPS is iNOS mediated, probably through S-nitrosation of proteins of early steps of insulin signalling.
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