Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/105774
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampRopelle, Eduardo Rochelept_BR
dc.contributor.authorunicampMoraes, Juliana Continpt_BR
dc.contributor.authorunicampPauli, José Rodrigopt_BR
dc.contributor.authorunicampCarvalho-Filho, Marco Antoniopt_BR
dc.contributor.authorunicampCintra, Dennys Esper Corrêapt_BR
dc.contributor.authorunicampVelloso, Lício Augustopt_BR
dc.contributor.authorunicampCarvalheira, José Barreto Campello Cavalheirapt_BR
dc.contributor.authorunicampSaad, Mário José Abdallapt_BR
dc.typeArtigopt_BR
dc.titleAcute physical exercise reverses S-nitrosation of the insulin receptor, insulin receptor substrate 1 and protein kinase B/akt in diet-induced obese wistar ratspt_BR
dc.contributor.authorRopelle, E.R.pt_BR
dc.contributor.authorMoraes, J.C.pt_BR
dc.contributor.authorPauli, J.R.pt_BR
dc.contributor.authorDe Souza, C.T.pt_BR
dc.contributor.authorCarvalho, Filho M.A.pt_BR
dc.contributor.authorCintra, D.E.pt_BR
dc.contributor.authorVelloso, L.A.pt_BR
dc.contributor.authorCarvalheira, J.B.C.pt_BR
dc.contributor.authorSaad, M.J.A.pt_BR
dc.subjectInibidores enzimáticospt_BR
dc.subjectResistência à insulinapt_BR
dc.subjectModelos animais de doençaspt_BR
dc.subject.otherlanguageDisease models, animalpt_BR
dc.subject.otherlanguageEnzyme inhibitorspt_BR
dc.subject.otherlanguageInsulin resistancept_BR
dc.description.abstractEarly evidence demonstrates that exogenous nitric oxide (NO) and the NO produced by inducible nitric oxide synthase (iNOS) can induce insulin resistance. Here, we investigated whether this insulin resistance, mediated by S-nitrosation of proteins involved in early steps of the insulin signal transduction pathway, could be reversed by acute physical exercise. Rats on a high-fat diet were subjected to swimming for two 3 h-long bouts, separated by a 45 min rest period. Two or 16 h after the exercise protocol the rats were killed and proteins from the insulin signalling pathway were analysed by immunoprecipitation and immunoblotting. We demonstrated that a high-fat diet led to an increase in the iNOS protein level and S-nitrosation of insulin receptor beta (IR beta), insulin receptor substrate 1 (IRS1) and Akt. Interestingly, an acute bout of exercise reduced iNOS expression and S-nitrosation of proteins involved in the early steps of insulin action, and improved insulin sensitivity in diet-induced obesity rats. Furthermore, administration of GSNO (NO donor) prevents this improvement in insulin action and the use of an inhibitor of iNOS (L-N6-(1-iminoethyl)lysine; L-NIL) simulates the effects of exercise on insulin action, insulin signalling and S-nitrosation of IR beta, IRS1 and Akt. In summary, a single bout of exercise reverses insulin sensitivity in diet-induced obese rats by improving the insulin signalling pathway, in parallel with a decrease in iNOS expression and in the S-nitrosation of IR/IRS1/Akt. The decrease in iNOS protein expression in the muscle of diet-induced obese rats after an acute bout of exercise was accompanied by an increase in AMP-activated protein kinase (AMPK) activity. These results provide new insights into the mechanism by which exercise restores insulin sensitivitypt
dc.relation.ispartofJournal of physiologypt_BR
dc.relation.ispartofabbreviationJ. physiol.pt_BR
dc.publisher.cityChichesterpt_BR
dc.publisher.countryReino Unidopt_BR
dc.publisherWileypt_BR
dc.date.issued2008pt_BR
dc.identifier.citationJournal Of Physiology. , v. 586, n. 2, p. 659 - 671, 2008.pt_BR
dc.language.isoengpt_BR
dc.description.volume586pt_BR
dc.description.issuenumber2pt_BR
dc.description.firstpage659pt_BR
dc.description.lastpage671pt_BR
dc.rightsfechadopt_BR
dc.sourceScopuspt_BR
dc.identifier.issn0022-3751pt_BR
dc.identifier.eissn1469-7793pt_BR
dc.identifier.doi10.1113/jphysiol.2007.142414pt_BR
dc.identifier.urlhttps://physoc.onlinelibrary.wiley.com/doi/full/10.1113/jphysiol.2007.142414pt_BR
dc.description.sponsorshipCONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQpt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.description.sponsorship1FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOpt_BR
dc.description.sponsorship1CNPQ – CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICOpt_BR
dc.description.sponsordocumentnumbersem informaçãopt_BR
dc.description.sponsordocumentnumbersem informaçãopt_BR
dc.date.available2015-06-30T19:19:41Z
dc.date.available2015-11-26T14:42:03Z-
dc.date.accessioned2015-06-30T19:19:41Z
dc.date.accessioned2015-11-26T14:42:03Z-
dc.description.provenanceMade available in DSpace on 2015-06-30T19:19:41Z (GMT). No. of bitstreams: 0 Previous issue date: 2008. Added 1 bitstream(s) on 2020-05-19T14:30:08Z : No. of bitstreams: 1 2-s2.0-38149095759.pdf: 643856 bytes, checksum: 642926ad8f3e69367bd6597706906e80 (MD5)en
dc.description.provenanceMade available in DSpace on 2015-11-26T14:42:03Z (GMT). No. of bitstreams: 0 Previous issue date: 2008en
dc.identifier.urihttp://www.repositorio.unicamp.br/handle/REPOSIP/105774
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/105774-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.identifier.source2-s2.0-38149095759-
dc.creator.orcid0000-0003-1655-9557pt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcid0000-0002-6129-1521pt_BR
dc.creator.orcid0000-0001-7008-4092pt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcid0000-0002-4806-7218pt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcid0000-0003-4544-6105pt_BR
dc.type.formArtigo originalpt_BR
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