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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/44510
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dc.creatorLeandro Ceotto Freitas Limapt_BR
dc.creatorEduardo Merlopt_BR
dc.creatorMarina Campos Zickerpt_BR
dc.creatorJuliana Maria Navia-Pelaezpt_BR
dc.creatorMiriane de Oliveirapt_BR
dc.creatorLuciano dos Santos Aggum Capettinipt_BR
dc.creatorCélia Regina Nogueirapt_BR
dc.creatorAdaliene Versiani Matos Ferreirapt_BR
dc.creatorSérgio Henrique Sousa Santospt_BR
dc.creatorJones Bernardes Gracelipt_BR
dc.date.accessioned2022-08-24T13:56:48Z-
dc.date.available2022-08-24T13:56:48Z-
dc.date.issued2018-12-15-
dc.citation.volume299pt_BR
dc.citation.spage21pt_BR
dc.citation.epage31pt_BR
dc.identifier.doihttps://doi.org/10.1016/j.toxlet.2018.08.018pt_BR
dc.identifier.issn0378-4274pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/44510-
dc.description.resumoWhite adipose tissue (WAT) dysfunction and obesity are a consequence of a low-grade inflammation state. These WAT irregularities could result from abnormal metabolic renin-angiotensin system (RAS) control. Recently, tributyltin (TBT) has been found to play a critical role in these metabolic irregularities. However, TBT actions on the WAT-RAS functions are not currently well understood. In this study, we assessed whether TBT exposure resulted in metabolic syndrome (MetS) development and other metabolic complications as a result of abnormal modulation of WAT-RAS pathways. TBT (100 ng/kg/day) was administered to adult female Wistar rats, and their WAT morphophysiology and adipokine profiles were assessed. We further assessed the expression of Angiotensin-II receptor proteins (AT1R and AT2R) and proteins involved in downstream pathways mediating inflammation and adipogenesis modulation. TBT-exposed rats exhibited increases in body weight and adiposity. TBT rats present dyslipidemia and insulin resistance, suggesting MetS development. TBT promoted WAT inflammatory infiltration, AT1R protein overexpression and reduced Angiotensin-(1–7) expression. These TBT WAT abnormalities are reflected by NFκB activation, with higher adipokine levels (leptin, TNF-α and IL-6) and overexpression of AKT, ERK, P38, FAS and PPARγ protein. In vitro, TBT exposure stimulates lipid accumulation, reduces AT2R protein expression, and increases leptin, AKT and ERK protein expression in 3T3L1 cells. These findings suggest that TBT exposure participates in MetS development via the improper function of WAT-RAS metabolic control.pt_BR
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorshipOutra Agênciapt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICA - INSTITUTO DE CIÊNCIAS AGRÁRIASpt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofToxicology Letterspt_BR
dc.rightsAcesso Abertopt_BR
dc.subject.otherObesidadept_BR
dc.subject.otherSíndrome metabólicapt_BR
dc.subject.otherSistema renina-angiotensinapt_BR
dc.subject.otherTecido adiposopt_BR
dc.titleTributyltin impacts in metabolic syndrome development through disruption of angiotensin II receptor signaling pathways in white adipose tissue from adult female ratspt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.sciencedirect.com/science/article/pii/S0378427418318265?via%3Dihubpt_BR
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