Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/35272
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dc.contributor.authorMori, Marcelo A. [UNIFESP]
dc.contributor.authorSales, Vicencia Micheline [UNIFESP]
dc.contributor.authorMotta, Fabiana Louise [UNIFESP]
dc.contributor.authorFonseca, Raphael Gomes [UNIFESP]
dc.contributor.authorAlenina, Natalia
dc.contributor.authorGuadagnini, Dioze
dc.contributor.authorSchadock, Ines
dc.contributor.authorSilva, Elton Dias [UNIFESP]
dc.contributor.authorTorres, Hugo Arruda de Moura [UNIFESP]
dc.contributor.authorSantos, Edson Lucas dos [UNIFESP]
dc.contributor.authorCastro, Charlles Heldan [UNIFESP]
dc.contributor.authorD'Almeida, Vania [UNIFESP]
dc.contributor.authorAndreotti, Sandra
dc.contributor.authorCampana, Amanda Baron
dc.contributor.authorSertie, Rogerio A. L.
dc.contributor.authorSaad, Mario J. A.
dc.contributor.authorLima, Fabio Bessa
dc.contributor.authorBader, Michael
dc.contributor.authorPesquero, João Bosco [UNIFESP]
dc.date.accessioned2016-01-24T14:27:42Z-
dc.date.available2016-01-24T14:27:42Z-
dc.date.issued2012-09-14
dc.identifierhttp://dx.doi.org/10.1371/journal.pone.0044782
dc.identifier.citationPlos One. San Francisco: Public Library Science, v. 7, n. 9, 11 p., 2012.
dc.identifier.issn1932-6203
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/35272-
dc.description.abstractBackground: Kinins participate in the pathophysiology of obesity and type 2 diabetes by mechanisms which are not fully understood. Kinin B-1 receptor knockout mice (B-1(-/-)) are leaner and exhibit improved insulin sensitivity.Methodology/Principal Findings: Here we show that kinin B-1 receptors in adipocytes play a role in controlling whole body insulin action and glucose homeostasis. Adipocytes isolated from mouse white adipose tissue (WAT) constitutively express kinin B-1 receptors. in these cells, treatment with the B-1 receptor agonist des-Arg(9)-bradykinin improved insulin signaling, GLUT4 translocation, and glucose uptake. Adipocytes from B-1(-/-) mice showed reduced GLUT4 expression and impaired glucose uptake at both basal and insulin-stimulated states. To investigate the consequences of these phenomena to whole body metabolism, we generated mice where the expression of the kinin B-1 receptor was limited to cells of the adipose tissue (aP2-B-1/B-1(-/-)). Similarly to B-1(-/-) mice, aP2-B-1/B-1(-/-) mice were leaner than wild type controls. However, exclusive expression of the kinin B1 receptor in adipose tissue completely rescued the improved systemic insulin sensitivity phenotype of B-1(-/-) mice. Adipose tissue gene expression analysis also revealed that genes involved in insulin signaling were significantly affected by the presence of the kinin B-1 receptor in adipose tissue. in agreement, GLUT4 expression and glucose uptake were increased in fat tissue of aP2-B-1/B-1(-/-) when compared to B-1(-/-) mice. When subjected to high fat diet, aP2-B-1/B-1(-/-) mice gained more weight than B-1(-/-) littermates, becoming as obese as the wild types.Conclusions/Significance: Thus, kinin B-1 receptor participates in the modulation of insulin action in adipocytes, contributing to systemic insulin sensitivity and predisposition to obesity.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipDeutsche Forschungsgemeinschaft
dc.description.sponsorshipGerman Ministry of Education and Science
dc.format.extent11
dc.language.isoeng
dc.publisherPublic Library Science
dc.relation.ispartofPlos One
dc.rightsAcesso aberto
dc.titleKinin B1 Receptor in Adipocytes Regulates Glucose Tolerance and Predisposition to Obesityen
dc.typeArtigo
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionMax Delbruck Ctr Mol Med MDC
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.description.affiliationUniversidade Federal de São Paulo, Dept Biophys, São Paulo, Brazil
dc.description.affiliationMax Delbruck Ctr Mol Med MDC, Berlin, Germany
dc.description.affiliationUniv Estadual Campinas, Dept Internal Med, Campinas, SP, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Med, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Biosci, São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Dept Physiol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Biophys, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Med, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Biosci, São Paulo, Brazil
dc.description.sponsorshipIDDeutsche Forschungsgemeinschaft: BA1374/16-1
dc.description.sponsorshipIDGerman Ministry of Education and Science: BRA09/014
dc.identifier.fileWOS000308860100020.pdf
dc.identifier.doi10.1371/journal.pone.0044782
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000308860100020
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