Exercise training prevents hyperinsulinemia, muscular glycogen loss and muscle atrophy induced by dexamethasone treatment

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dc.contributor.authorBarel, Matheus [UNESP]
dc.contributor.authorBrogin Perez, Otavio Andre [UNESP]
dc.contributor.authorGiozzet, Vanessa Aparecida [UNESP]
dc.contributor.authorRafacho, Alex [UNESP]
dc.contributor.authorBosqueiro, José Roberto [UNESP]
dc.contributor.authorAmaral, Sandra Lia do [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:26:07Z
dc.date.available2014-05-20T13:26:07Z
dc.date.issued2010-03-01
dc.description.abstractThis study investigated whether exercise training could prevent the negative side effects of dexamethasone. Rats underwent a training period and were either submitted to a running protocol (60% physical capacity, 5 days/week for 8 weeks) or kept sedentary. After this training period, the animals underwent dexamethasone treatment (1 mg/kg per day, i.p., 10 days). Glycemia, insulinemia, muscular weight and muscular glycogen were measured from blood and skeletal muscle. Vascular endothelial growth factor (VEGF) protein was analyzed in skeletal muscles. Dexamethasone treatment evoked body weight loss (-24%), followed by muscular atrophy in the tibialis anterior (-25%) and the extensor digitorum longus (EDL, -15%). Dexamethasone also increased serum insulin levels by 5.7-fold and glucose levels by 2.5-fold compared to control. The exercise protocol prevented atrophy of the EDL and insulin resistance. Also, dexamethasone-treated rats showed decreased muscular glycogen (-41%), which was further attenuated by the exercise protocol. The VEGF protein expression decreased in the skeletal muscles of dexamethasone-treated rats and was unaltered by the exercise protocol. These data suggest that exercise attenuates hyperglycemia and may also prevent insulin resistance, muscular glycogen loss and muscular atrophy, thus suggesting that exercise may have some benefits during glucocorticoid treatment.en
dc.description.affiliationSão Paulo State Univ, UNESP, Sch Sci, Dept Phys Educ, Bauru, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ, UNESP, Sch Sci, Dept Phys Educ, Bauru, SP, Brazil
dc.description.sponsorshipMatheus Barel
dc.description.sponsorshipOtavio Andre Brogin Perez
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipFundação para o Desenvolvimento da UNESP (FUNDUNESP)
dc.description.sponsorshipIdMatheus Barel: 06/51936-2
dc.description.sponsorshipIdOtavio Andre Brogin Perez: 06/51935-6
dc.description.sponsorshipIdFUNDUNESP: 00540/06
dc.format.extent999-1007
dc.identifierhttp://dx.doi.org/10.1007/s00421-009-1272-6
dc.identifier.citationEuropean Journal of Applied Physiology. New York: Springer, v. 108, n. 5, p. 999-1007, 2010.
dc.identifier.doi10.1007/s00421-009-1272-6
dc.identifier.issn1439-6319
dc.identifier.lattes2423477869556138
dc.identifier.urihttp://hdl.handle.net/11449/8367
dc.identifier.wosWOS:000274957600012
dc.language.isoeng
dc.publisherSpringer
dc.relation.ispartofEuropean Journal of Applied Physiology
dc.relation.ispartofjcr2.401
dc.relation.ispartofsjr1,186
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectInsulin resistanceen
dc.subjectDexamethasoneen
dc.subjectExercise training and skeletal muscleen
dc.titleExercise training prevents hyperinsulinemia, muscular glycogen loss and muscle atrophy induced by dexamethasone treatmenten
dc.typeArtigo
dcterms.licensehttp://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0
dcterms.rightsHolderSpringer
unesp.author.lattes2423477869556138
unesp.author.orcid0000-0001-9473-3739[6]
unesp.author.orcid0000-0002-8637-6097[4]
unesp.author.orcid0000-0001-5367-7427[5]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Ciências, Baurupt
unesp.departmentEducação Física - FCpt

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