Endurance training improves responsiveness to insulin and modulates insulin signal transduction through the phosphatidylinositol 3-kinase/Akt-1 pathway

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dc.contributor.authorLuciano, E.
dc.contributor.authorCarneiro, E. M.
dc.contributor.authorCarvalho, CRO
dc.contributor.authorCarvalheira, JBC
dc.contributor.authorPeres, S. B.
dc.contributor.authorReis, MAB
dc.contributor.authorSaad, MJA
dc.contributor.authorBoschero, A. C.
dc.contributor.authorVelloso, L. A.
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-02-26T17:14:31Z
dc.date.accessioned2014-05-20T13:57:53Z
dc.date.available2014-02-26T17:14:31Z
dc.date.available2014-05-20T13:57:53Z
dc.date.issued2002-07-01
dc.description.abstractBackground: Endurance training increases insulin-stimulated muscle glucose transport and leads to improved metabolic control in diabetic patients.Objective: To analyze the effects of endurance training on the early steps of insulin action in muscle of rats. Design: Male rats submitted to daily swimming for 6 weeks were compared with sedentary controls. At the end of the training period, anesthetized animals received an intravenous (i.v.) injection of insulin and had a fragment of their gastrocnemius muscle excised for the experiments.Methods: Associations between insulin receptor, insulin receptor substrates (IRS)-1 and -2 and phosphatidylinositol 3-kinase (PI3-kinase) were analyzed by immunoprecipitation and immunoblotting. Akt-1 serine phosphorylation and specific protein quantification were detected by immunoblotting of total extracts, and IRS-1/IRS-2-associated PI3-kinase activity were determined by thin-layer chromatography.Results: Insulin-induced phosphorylation of IRS-1 and IRS-2 increased respectively by 1.8-fold (P < 0.05) and 1.5-fold (P < 0.05), whereas their association with PI3-kinase increased by 2.3-fold (P < 0.05) and 1.9-fold (P < 0.05) in trained rats as compared with sedentary controls, respectively. The activity of PI3-kinase associated with IRS-1 and IRS-2 increased by 1.8-fold (P < 0.05) and 1.7-fold (P < 0.05) respectively, in trained rats as compared with their untrained counterparts. Serine phosphorylation of Akt-1/PKB increased 1.7-fold (P < 0.05) in trained rats in response to insulin. These findings were accompanied by increased responsiveness to insulin as demonstrated by a reduced area under the curve for insulin during an i.v. glucose tolerance test, by increased glucose disappearance rate during an insulin tolerance test, and by increased expression of glucose transporter-4.Conclusions: the increased responsiveness to insulin induced by chronic exercise in rat skeletal muscle may result, at least in part, from the modulation of the insulin signaling pathway at different molecular levels.en
dc.description.affiliationUNICAMP, Dept Internal Med, BR-13081970 Campinas, SP, Brazil
dc.description.affiliationUNICAMP, Dept Physiol & Biophys, BR-13081970 Campinas, SP, Brazil
dc.description.affiliationState Univ São Paulo, UNESP, Dept Phys Educ, Rio Claro, Brazil
dc.description.affiliationUnespState Univ São Paulo, UNESP, Dept Phys Educ, Rio Claro, Brazil
dc.format.extent149-157
dc.identifierhttp://dx.doi.org/10.1530/eje.0.1470149
dc.identifier.citationEuropean Journal of Endocrinology. Bristol: Bio Scientifica Ltd, v. 147, n. 1, p. 149-157, 2002.
dc.identifier.doi10.1530/eje.0.1470149
dc.identifier.issn0804-4643
dc.identifier.lattes2933779830637191
dc.identifier.urihttp://hdl.handle.net/11449/20618
dc.identifier.wosWOS:000178743500019
dc.language.isoeng
dc.publisherBio Scientifica Ltd
dc.relation.ispartofEuropean Journal of Endocrinology
dc.relation.ispartofjcr4.333
dc.relation.ispartofsjr1,892
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.titleEndurance training improves responsiveness to insulin and modulates insulin signal transduction through the phosphatidylinositol 3-kinase/Akt-1 pathwayen
dc.typeArtigo
dcterms.licensehttp://www.eje-online.org/site/misc/archiving_policy.xhtml
dcterms.rightsHolderBio Scientifica Ltd
unesp.author.lattes2933779830637191
unesp.author.orcid0000-0001-5824-8656[3]
unesp.author.orcid0000-0002-0136-0943[4]
unesp.author.orcid0000-0003-3829-8570[8]
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Rio Claropt

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