Tributyltin impacts in metabolic syndrome development through disruption of angiotensin II receptor signaling pathways in white adipose tissue from adult female rats

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dc.creatorLeandro Ceotto Freitas Lima
dc.creatorEduardo Merlo
dc.creatorMarina Campos Zicker
dc.creatorJuliana Maria Navia-Pelaez
dc.creatorMiriane de Oliveira
dc.creatorLuciano dos Santos Aggum Capettini
dc.creatorCélia Regina Nogueira
dc.creatorAdaliene Versiani Matos Ferreira
dc.creatorSérgio Henrique Sousa Santos
dc.creatorJones Bernardes Graceli
dc.date.accessioned2022-08-24T13:56:48Z
dc.date.accessioned2025-09-08T23:40:22Z
dc.date.available2022-08-24T13:56:48Z
dc.date.issued2018-12-15
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico
dc.description.sponsorshipOutra Agência
dc.identifier.doihttps://doi.org/10.1016/j.toxlet.2018.08.018
dc.identifier.issn0378-4274
dc.identifier.urihttps://hdl.handle.net/1843/44510
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofToxicology Letters
dc.rightsAcesso Aberto
dc.subjectObesidade
dc.subjectSíndrome metabólica
dc.subjectSistema renina-angiotensina
dc.subjectTecido adiposo
dc.titleTributyltin impacts in metabolic syndrome development through disruption of angiotensin II receptor signaling pathways in white adipose tissue from adult female rats
dc.typeArtigo de periódico
local.citation.epage31
local.citation.spage21
local.citation.volume299
local.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.
local.publisher.countryBrasil
local.publisher.departmentICA - INSTITUTO DE CIÊNCIAS AGRÁRIAS
local.publisher.initialsUFMG
local.url.externahttps://www.sciencedirect.com/science/article/pii/S0378427418318265?via%3Dihub

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