Tributyrin attenuates metabolic and inflammatory changes associated with obesity through a GPR109A-dependent mechanism

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dc.contributor.authorSato, Fabio Takeopt_BR
dc.contributor.authorYap, Yu Annept_BR
dc.contributor.authorCrisma, Amanda Rabellopt_BR
dc.contributor.authorPortovedo, Marianapt_BR
dc.contributor.authorMurata, Gilson Masahiropt_BR
dc.contributor.authorHirabara, Sandro Massaopt_BR
dc.contributor.authorRibeiro, Willian Rodriguespt_BR
dc.contributor.authorFerreira, Caroline Marcantoniopt_BR
dc.contributor.authorCruz, Maysa Marianapt_BR
dc.contributor.authorPereira, Joice Naiara Bertagliapt_BR
dc.contributor.authorPayolla, Tanyara Balianipt_BR
dc.contributor.authorGuima, Suzana Eiko Satopt_BR
dc.contributor.authorThomas, Andrew Maltezpt_BR
dc.contributor.authorSetubal, João Carlospt_BR
dc.contributor.authorAlonso-Vale, Maria Isabel Cardosopt_BR
dc.contributor.authorSantos, Marinilce Fagundespt_BR
dc.contributor.authorCuri, Ruipt_BR
dc.contributor.authorMarino, Elianapt_BR
dc.contributor.authorVinolo, Marco A. R.pt_BR
dc.date.accessioned2020-09-08T18:28:28Z-
dc.date.available2020-09-08T18:28:28Z-
dc.date.issued2020pt_BR
dc.identifier.citationSato FT, Yap YA, Crisma AR, Portovedo M, Murata GM, Hirabara SM, et al. Tributyrin attenuates metabolic and inflammatory changes associated with obesity through a GPR109A-dependent mechanism. Cells. 2020 Sep;9(9):2007. doi:10.3390/cells9092007.pt_BR
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/3181-
dc.description.abstractObesity is linked with altered microbial short-chain fatty acids (SCFAs), which are a signature of gut dysbiosis and inflammation. In the present study, we investigated whether tributyrin, a prodrug of the SCFA butyrate, could improve metabolic and inflammatory profiles in diet-induced obese mice. Mice fed a high-fat diet for eight weeks were treated with tributyrin or placebo for another six weeks. We show that obese mice treated with tributyrin had lower body weight gain and an improved insulin responsiveness and glucose metabolism, partly via reduced hepatic triglycerides content. Additionally, tributyrin induced an anti-inflammatory state in the adipose tissue by reduction of Il-1β and Tnf-a and increased Il-10, Tregs cells and M2-macrophages. Moreover, improvement in glucose metabolism and reduction of fat inflammatory states associated with tributyrin treatment were dependent on GPR109A activation. Our results indicate that exogenous targeting of SCFA butyrate attenuates metabolic and inflammatory dysfunction, highlighting a potentially novel approach to tackle obesitypt_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)pt_BR
dc.format.extent2007pt_BR
dc.language.isoEnglishpt_BR
dc.relation.ispartofCellspt_BR
dc.rightsOpen Accesspt_BR
dc.titleTributyrin attenuates metabolic and inflammatory changes associated with obesity through a GPR109A-dependent mechanismpt_BR
dc.typeArticlept_BR
dc.identifier.doi10.3390/cells9092007pt_BR
dc.identifier.urlhttps://doi.org/10.3390/cells9092007pt_BR
dc.contributor.externalUniversidade Estadual de Campinas (UNICAMP)pt_BR
dc.contributor.externalMonash Universitypt_BR
dc.contributor.externalUniversidade Federal do Paraná (UFPR)pt_BR
dc.contributor.externalUniversidade de São Paulo (USP)pt_BR
dc.contributor.externalUniversidade Cruzeiro do Sul (UNICSUL)pt_BR
dc.contributor.externalUniversidade Federal de São Paulo (UNIFESP)pt_BR
dc.identifier.citationvolume9pt_BR
dc.identifier.citationissue9pt_BR
dc.subject.keywordbutyratept_BR
dc.subject.keywordmicrobiotapt_BR
dc.subject.keywordinsulin resistancept_BR
dc.subject.keyworddysbiosispt_BR
dc.relation.ispartofabbreviatedCellspt_BR
dc.identifier.citationabntv. 9, n. 9, 2007, set. 2020pt_BR
dc.identifier.citationvancouver2020 Sep;9(9):2007pt_BR
dc.contributor.butantanCuri, Rui|:Diretorpt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦12/10653-9pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦18/15313-8pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2012/15774-9pt_BR
dc.sponsorship.butantanConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)¦¦14/2011pt_BR
dc.sponsorship.butantanCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)¦¦001pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
dc.description.dbindexedYespt_BR
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