Functional alterations in endocrine pancreas of rats with different degrees of dexamethasone-induced insulin resistance

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dc.contributor.authorRafacho, Alex
dc.contributor.authorGiozzet, Vanessa A. G.
dc.contributor.authorBoschero, Antonio C.
dc.contributor.authorBosqueiro, José Roberto [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.date.accessioned2014-05-20T13:26:07Z
dc.date.available2014-05-20T13:26:07Z
dc.date.issued2008-04-01
dc.description.abstractObjectives: We have analyzed the peripheral insulin and glucose sensitivity in vivo, and islet function ex vivo in rats with different degrees of insulin resistance induced by dexamethasone (DEX).Methods: Dexamethasone, in the concentrations of 0.1 (DEX 0.1), 0.5 (DEX 0.5), and 1.0 mg/kg body weight (DEX 1.0) was administered daily, intraperitoneally, to adult Wistar rats for 5 days, whereas controls received saline.Results: Dexamethasone treatment induced peripheral insulin resistance in a dose-dependent manner. At the end of the treatment, only DEX 1.0 rats showed significant increase of postabsorptive blood glucose and serum triglycerides, and nonesterified fatty acids levels. Incubation of pancreatic islets in increasing glucose concentrations (2.8-22 mM) led to an augmented insulin secretion in all DEX-treated rats. Leucine, carbachol, and high KCl concentrations induced the insulin release in DEX 0.5 and DEX 1.0, whereas arginine augmented secretion in all DEX-treated groups.Conclusions: We demonstrate that in DEX 0.5 and, especially in DEX 0.1 groups, but not in DEX 1.0, the adaptations that occurred in the endocrine pancreas are able to counteract metabolic disorders (glucose intolerance and dyslipidemia). These animal models seem to be interesting approaches for the study of degrees of subjacent effects that may mediate type 2 diabetes (DEX 1.0) and islet function alterations, without collateral effects (DEX 0.1 and DEX 0.5).en
dc.description.affiliationUNESP, Fac Ciencias, Dept Educ Fis, BR-17033360 Bauru, SP, Brazil
dc.description.affiliationUniv Estadual Campinas, Inst Biol, Dept Physiol & Biophys, Campinas, SP, Brazil
dc.description.affiliationUnespUNESP, Fac Ciencias, Dept Educ Fis, BR-17033360 Bauru, SP, Brazil
dc.format.extent284-293
dc.identifierhttp://dx.doi.org/10.1097/MPA.0b013e31815ba826
dc.identifier.citationPancreas. Philadelphia: Lippincott Williams & Wilkins, v. 36, n. 3, p. 284-293, 2008.
dc.identifier.doi10.1097/MPA.0b013e31815ba826
dc.identifier.issn0885-3177
dc.identifier.lattes2423477869556138
dc.identifier.urihttp://hdl.handle.net/11449/8368
dc.identifier.wosWOS:000254589700010
dc.language.isoeng
dc.publisherLippincott Williams & Wilkins
dc.relation.ispartofPancreas
dc.relation.ispartofjcr2.958
dc.relation.ispartofsjr1,327
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectglucocorticoidsen
dc.subjectglucose and insulin sensitivityen
dc.subjectinsulin secretionen
dc.subjectpancreatic isletsen
dc.subjectplasma lipidsen
dc.titleFunctional alterations in endocrine pancreas of rats with different degrees of dexamethasone-induced insulin resistanceen
dc.typeArtigo
dcterms.licensehttp://edmgr.ovid.com/spine/accounts/copyrightTransfer.pdf
dcterms.rightsHolderLippincott Williams & Wilkins
unesp.author.lattes2423477869556138
unesp.author.orcid0000-0003-3829-8570[3]
unesp.author.orcid0000-0002-8637-6097[1]
unesp.author.orcid0000-0001-5367-7427[4]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Ciências, Baurupt
unesp.departmentEducação Física - FCpt

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