Use este identificador para citar ou linkar para este item:
http://hdl.handle.net/1843/44510
Tipo: | Artigo de Periódico |
Título: | Tributyltin impacts in metabolic syndrome development through disruption of angiotensin II receptor signaling pathways in white adipose tissue from adult female rats |
Autor(es): | Leandro Ceotto Freitas Lima Eduardo Merlo Marina Campos Zicker Juliana Maria Navia-Pelaez Miriane de Oliveira Luciano dos Santos Aggum Capettini Célia Regina Nogueira Adaliene Versiani Matos Ferreira Sérgio Henrique Sousa Santos Jones Bernardes Graceli |
Resumo: | White 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. |
Assunto: | Obesidade Síndrome metabólica Sistema renina-angiotensina Tecido adiposo |
Idioma: | eng |
País: | Brasil |
Editor: | Universidade Federal de Minas Gerais |
Sigla da Instituição: | UFMG |
Departamento: | ICA - INSTITUTO DE CIÊNCIAS AGRÁRIAS |
Tipo de Acesso: | Acesso Aberto |
Identificador DOI: | https://doi.org/10.1016/j.toxlet.2018.08.018 |
URI: | http://hdl.handle.net/1843/44510 |
Data do documento: | 15-Dez-2018 |
metadata.dc.url.externa: | https://www.sciencedirect.com/science/article/pii/S0378427418318265?via%3Dihub |
metadata.dc.relation.ispartof: | Toxicology Letters |
Aparece nas coleções: | Artigo de Periódico |
Arquivos associados a este item:
Arquivo | Descrição | Tamanho | Formato | |
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Tributyltin impacts in metabolic syndrome development through disruption of angiotensin II receptor signaling pathways in white adipose tissue from adult female rats.pdf | 1.96 MB | Adobe PDF | Visualizar/Abrir |
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