Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/348304
Full metadata record
DC FieldValueLanguage
dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampBatista, Thiago Martins-
dc.contributor.authorunicampCarneiro, Everardo Magalhães-
dc.typeArtigopt_BR
dc.titleShort-term treatment with bisphenol-A leads to metabolic abnormalities in adult male micept_BR
dc.contributor.authorBatista, Thiago M.-
dc.contributor.authorAlonso-Magdalena, Paloma-
dc.contributor.authorVieira, Elaine-
dc.contributor.authorAmaral, Maria Esmeria C.-
dc.contributor.authorCederroth, Christopher R.-
dc.contributor.authorNef, Serge-
dc.contributor.authorQuesada, Ivan-
dc.contributor.authorCarneiro, Everardo M.-
dc.contributor.authorNadal, Angel-
dc.subjectBisfenol Apt_BR
dc.subject.otherlanguageBisphenol Apt_BR
dc.description.abstractBisphenol-A (BPA) is one of the most widespread endocrine disrupting chemicals (EDC) used as the base compound in the manufacture of polycarbonate plastics. Although evidence points to consider exposure to BPA as a risk factor for insulin resistance, its actions on whole body metabolism and on insulin-sensitive tissues are still unclear. The aim of the present work was to study the effects of low doses of BPA in insulin-sensitive peripheral tissues and whole body metabolism in adult mice. Adult mice were treated with subcutaneous injection of 100 mu g/kg BPA or vehicle for 8 days. Whole body energy homeostasis was assessed with in vivo indirect calorimetry. Insulin signaling assays were conducted by western blot analysis. Mice treated with BPA were insulin resistant and had increased glucose-stimulated insulin release. BPA-treated mice had decreased food intake, lower body temperature and locomotor activity compared to control. In skeletal muscle, insulin-stimulated tyrosine phosphorylation of the insulin receptor beta subunit was impaired in BPA-treated mice. This impairment was associated with a reduced insulin-stimulated Akt phosphorylation in the Thr(308) residue. Both skeletal muscle and liver displayed an upregulation of IRS-1 protein by BPA. The mitogen-activated protein kinase (MAPK) signaling pathway was also impaired in the skeletal muscle from BPA-treated mice. In the liver, BPA effects were of lesser intensity with decreased insulin-stimulated tyrosine phosphorylation of the insulin receptor b subunit. In conclusion, short-term treatment with low doses of BPA slows down whole body energy metabolism and disrupts insulin signaling in peripheral tissues. Thus, our findings support the notion that BPA can be considered a risk factor for the development of type 2 diabetespt_BR
dc.relation.ispartofPLoS onept_BR
dc.publisher.citySan Francisco, CApt_BR
dc.publisher.countryEstados Unidospt_BR
dc.publisherPublic Library of Sciencept_BR
dc.date.issued2012-
dc.date.monthofcirculationMar.pt_BR
dc.language.isoengpt_BR
dc.description.volume7pt_BR
dc.description.issuenumber3pt_BR
dc.rightsAbertopt_BR
dc.sourceWOSpt_BR
dc.identifier.eissn1932-6203pt_BR
dc.identifier.doi10.1371/journal.pone.0033814pt_BR
dc.identifier.urlhttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0033814pt_BR
dc.date.available2020-08-28T20:06:47Z-
dc.date.accessioned2020-08-28T20:06:47Z-
dc.description.provenanceSubmitted by Sanches Olivia (olivias@unicamp.br) on 2020-08-28T20:06:47Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-01-04T15:14:37Z : No. of bitstreams: 1 000304489000037.pdf: 590720 bytes, checksum: b0a212c59cf1365de6201ff236d36406 (MD5)en
dc.description.provenanceMade available in DSpace on 2020-08-28T20:06:47Z (GMT). No. of bitstreams: 0 Previous issue date: 2012en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/348304-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Biologia Estrutural e Funcionalpt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.identifier.source000304489000037pt_BR
dc.creator.orcid0000-0001-6971-1191pt_BR
dc.creator.orcid0000-0003-3212-369Xpt_BR
dc.type.formArtigo de pesquisapt_BR
dc.identifier.articleide33814pt_BR
dc.description.otherSponsorshipsem informaçãopt_BR
Appears in Collections:IB - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
000304489000037.pdf576.88 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.