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dc.contributor.CRUESPUNIVERSIDADE DE ESTADUAL DE CAMPINASpt_BR
dc.typeArtigo de periódicopt_BR
dc.titleCross-talk Between The Insulin And Leptin Signaling Systems In Rat Hypothalamus.pt_BR
dc.contributor.authorCarvalheira, José B Cpt_BR
dc.contributor.authorTorsoni, Márcio Apt_BR
dc.contributor.authorUeno, Mirianpt_BR
dc.contributor.authorAmaral, Maria Ept_BR
dc.contributor.authorAraújo, Eliana Ppt_BR
dc.contributor.authorVelloso, Lício Apt_BR
dc.contributor.authorGontijo, José A Rpt_BR
dc.contributor.authorSaad, Mario J Apt_BR
unicamp.authorJosé B C Carvalheira, Department of Internal Medicine, State University of Campinas (UNICAMP), Campinas SP, Brazil.pt_BR
unicamp.author.externalMárcio A Torsoni,pt
unicamp.author.externalMirian Ueno,pt
unicamp.author.externalMaria E Amaral,pt
unicamp.author.externalEliana P Araújo,pt
unicamp.author.externalLício A Velloso,pt
unicamp.author.externalJosé A R Gontijo,pt
unicamp.author.externalMario J A Saad,pt
dc.subjectAnimalspt_BR
dc.subjectBlotting, Westernpt_BR
dc.subjectDna-binding Proteinspt_BR
dc.subjectEatingpt_BR
dc.subjectHypothalamuspt_BR
dc.subjectInjections, Intraventricularpt_BR
dc.subjectInsulinpt_BR
dc.subjectInsulin Receptor Substrate Proteinspt_BR
dc.subjectIntracellular Signaling Peptides And Proteinspt_BR
dc.subjectLeptinpt_BR
dc.subjectMalept_BR
dc.subjectMitogen-activated Protein Kinasespt_BR
dc.subjectPhosphatidylinositol 3-kinasespt_BR
dc.subjectPhosphoproteinspt_BR
dc.subjectPhosphorylationpt_BR
dc.subjectProtein-serine-threonine Kinasespt_BR
dc.subjectProto-oncogene Proteinspt_BR
dc.subjectProto-oncogene Proteins C-aktpt_BR
dc.subjectRatspt_BR
dc.subjectRats, Wistarpt_BR
dc.subjectStat3 Transcription Factorpt_BR
dc.subjectSignal Transductionpt_BR
dc.subjectTrans-activatorspt_BR
dc.description.abstractTo investigate whether insulin and leptin share common intracellular signal transduction pathways and to determine whether these hormonal signaling systems modulate each other's action in rat hypothalamus. Male Wistar rats were studied after chronic implantation of an intracerebroventricular catheter into the third ventricle. Immunoprecipitation and immunoblotting were used to examine the activation of insulin and leptin signaling molecules in the rat hypothalamus. Insulin alone is able to produce molecular activation of insulin receptor substrates (IRSs)/phosphatidylinositol 3-kinase (PI 3-kinase)/Akt and mitogen-activated protein (MAP) kinase signaling pathways in hypothalamus, whereas leptin alone activates MAP kinase and IRSs/PI 3-kinase signaling with no effect on Akt. Combined infusion of leptin and insulin provokes a dual action. There was no quantitative potentialization of any single hormone's action on the elements of the insulin signaling pathway, IRSs/PI 3-kinase/Akt, and MAP kinase. Conversely, leptin plus insulin leads to quantitative potentialization of molecular signaling through the Janus kinase/signal transducer and activator of transcription pathway. We provide evidence for a convergence of leptin and insulin signaling at the level of IRSs-PI 3-kinase and a divergence at the level of Akt. Moreover, our results indicate a direct and positive cross-talk between insulin and leptin at the level of Janus kinase 2 and signal transducer and activator of transcription 3 tyrosine phosphorylation. This mechanism may serve to potentiate the activity of both insulin and leptin pathways and to increase stimulation in physiological processes such as the control of food intake and body weight, which are under the combined control of insulin and leptin.en
dc.relation.ispartofObesity Researchpt_BR
dc.relation.ispartofabbreviationObes. Res.pt_BR
dc.date.issued2005-Janpt_BR
dc.identifier.citationObesity Research. v. 13, n. 1, p. 48-57, 2005-Jan.pt_BR
dc.language.isoengpt_BR
dc.description.volume13pt_BR
dc.description.firstpage48-57pt_BR
dc.rightsfechadopt_BR
dc.sourcePubMedpt_BR
dc.identifier.issn1071-7323pt_BR
dc.identifier.doi10.1038/oby.2005.7pt_BR
dc.identifier.urlhttp://www.ncbi.nlm.nih.gov/pubmed/15761162pt_BR
dc.date.available2015-11-27T13:02:51Z-
dc.date.accessioned2015-11-27T13:02:51Z-
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dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/196618-
dc.identifier.idPubmed15761162pt_BR
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