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dc.contributor.CRUESPUniversidade Estadual de Campinaspt_BR
dc.typeArtigo de periódicopt_BR
dc.titleDexamethasone-induced insulin resistance is associated with increased connexin 36 mRNA and protein expression in pancreatic rat isletspt_BR
dc.contributor.authorRafacho, Apt_BR
dc.contributor.authorRoma, LPpt_BR
dc.contributor.authorTaboga, SRpt_BR
dc.contributor.authorBoschero, ACpt_BR
dc.contributor.authorBosqueiro, JRpt_BR
unicamp.author.emailbosqueir@fc.unesp.brpt_BR
unicamp.authorSao Paulo State Univ UNESP, Fac Sci, Dept Biol Sci, BR-17033360 Bauru, SP, Brazil Univ Estadual Campinas, Inst Biol, Dept Phys & Biophys, Campinas, SP, Brazil Sao Paulo State Univ UNESP, Inst Biosci Humanities & Exact Sci, Dept Biol, Sao Jose Do Rio Preto, SP, Brazilpt_BR
dc.subjectconnexinspt_BR
dc.subjectglucocorticoidspt_BR
dc.subjectinsulin resistancept_BR
dc.subjectglucose-stimulated insulin secretionpt_BR
dc.subjectpancreatic isletspt_BR
dc.subject.wosBeta-cell Dysfunctionpt_BR
dc.subject.wosTreated Ratspt_BR
dc.subject.wosPhosphatidylinositol 3-kinasept_BR
dc.subject.wosReceptor Substrate-1pt_BR
dc.subject.wosMembrane Channelspt_BR
dc.subject.wosMouse Isletspt_BR
dc.subject.wosAging Ratspt_BR
dc.subject.wosMin6 Cellspt_BR
dc.subject.wosIn-vitropt_BR
dc.subject.wosSecretionpt_BR
dc.description.abstractAugmented glucose-stimulated insulin secretion (GSIS) is an adaptive mechanism exhibited by pancreatic islets from insulin-resistant animal models. Gap junction proteins have been proposed to contribute to islet function. As such, we investigated the expression of connexin 36 (Cx36), connexin 43 (Cx43), and the glucose transporter Glut2 at mRNA and protein levels in pancreatic islets of dexamethasone (DEX)-induced insulin-resistant rats. Study rats received daily injections of DEX (1 mg/kg body mass, i.p.) for 5 days, whereas control rats (CTL) received saline solution. DEX rats exhibited peripheral insulin resistance, as indicated by the significant postabsorptive insulin levels and by the constant rate for glucose disappearance (K-ITT). GSIS was significantly higher in DEX islets (1.8-fold in 16.7 mmol/L glucose vs. CTL, p < 0.05). A significant increase of 2.25-fold in islet area was observed in DEX vs. CTL islets (p < 0.05). Cx36 mRNA expression was significantly augmented, Cx43 diminished, and Glut2 mRNA was unaltered in islets of DEX vs. CTL (p < 0.05). Cx36 protein expression was 1.6-fold higher than that of CTL islets (p < 0.05). Glut2 protein expression was unaltered and Cx43 was not detected at the protein level. We conclude that DEX-induced insulin resistance is accompanied by increased GSIS and this may be associated with increase of Cx36 protein expression.pt
dc.relation.ispartofCanadian Journal Of Physiology And Pharmacologypt_BR
dc.relation.ispartofabbreviationCan. J. Physiol. Pharmacol.pt_BR
dc.publisher.cityOttawapt_BR
dc.publisher.countryCanadápt_BR
dc.publisherNatl Research Council Canada-n R C Research Presspt_BR
dc.date.issued2007pt_BR
dc.date.monthofcirculationMAYpt_BR
dc.identifier.citationCanadian Journal Of Physiology And Pharmacology. Natl Research Council Canada-n R C Research Press, v. 85, n. 5, n. 536, n. 545, 2007.pt_BR
dc.language.isoenpt_BR
dc.description.volume85pt_BR
dc.description.issuenumber5pt_BR
dc.description.firstpage536pt_BR
dc.description.lastpage545pt_BR
dc.rightsfechadopt_BR
dc.sourceWeb of Sciencept_BR
unicamp.cruespUNESPpt_BR
dc.identifier.issn0008-4212pt_BR
dc.identifier.wosidWOS:000249010900008pt_BR
dc.identifier.doi10.1139/Y07-037pt_BR
dc.date.available2014-11-15T10:06:23Z
dc.date.available2015-11-26T17:19:29Z-
dc.date.accessioned2014-11-15T10:06:23Z
dc.date.accessioned2015-11-26T17:19:29Z-
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dc.description.provenanceMade available in DSpace on 2015-11-26T17:19:29Z (GMT). No. of bitstreams: 2 WOS000249010900008.pdf: 4541936 bytes, checksum: 9b14b3a9206039efcd847aabf89248c8 (MD5) WOS000249010900008.pdf.txt: 10 bytes, checksum: 2c6eb67c8897d916ae47524b1a844d3f (MD5) Previous issue date: 2007en
dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/61649pt_BR
dc.identifier.urihttp://www.repositorio.unicamp.br/handle/REPOSIP/61649
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/61649-
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