Artículos de revistas
Targeted Disruption Of Inos Prevents Lps-induced S-nitrosation Of Irbeta/irs-1 And Akt And Insulin Resistance In Muscle Of Mice.
Registro en:
American Journal Of Physiology. Endocrinology And Metabolism. v. 291, n. 3, p. E476-82, 2006-Sep.
0193-1849
10.1152/ajpendo.00422.2005
16638822
Autor
Carvalho-Filho, Marco A
Ueno, Mirian
Carvalheira, José B C
Velloso, Lício A
Saad, Mario J A
Institución
Resumen
We have previously demonstrated that the insulin resistance associated with inducible nitric oxide synthase (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 beta-subunit (IRbeta), insulin receptor substrate 1(IRS-1), and Akt. S-nitrosation of IRbeta and Akt impairs their kinase activities, and S-nitrosation of IRS-1 reduces its tissue expression. 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 IRbeta 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 IRbeta/IRS-1 and Akt. In the muscle of iNOS(-/-) mice, we did not observe enhanced iNOS expression or any S-nitrosation of IRbeta/IRS-1 and Akt after LPS treatment. Moreover, insulin resistance was not present. The preservation of insulin-induced tyrosine phosphorylation of IRbeta 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 signaling. 291 E476-82
Materias
Ítems relacionados
Mostrando ítems relacionados por Título, autor o materia.
-
Glucose-induced Insulin Secretion Is Impaired And Insulin-induced Phosphorylation Of The Insulin Receptor And Insulin Receptor Substrate-1 Are Increased In Protein-deficient Rats
Reis M.A.B.; Carneiro E.M.; Mello M.A.R.; Boschero A.C.; Saad M.J.A.; Velloso L.A. -
Glucose-induced insulin secretion is impaired and insulin-induced phosphorylation of the insulin receptor and insulin receptor substrate-1 are increased in protein-deficient rats
Reis, Marise A.B.; Carneiro, Everardo M.; Mello, Maria A.R.; Boschero, A. Carlos; Saad, Mario J. A.; Velloso, Licio A. -
Glucose-induced Insulin Secretion Is Impaired And Insulin-induced Phosphorylation Of The Insulin Receptor And Insulin Receptor Substrate-1 Are Increased In Protein-deficient Rats.
Reis, M A; Carneiro, E M; Mello, M A; Boschero, A C; Saad, M J; Velloso, L A