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Tributyrin Attenuates Metabolic and Inflammatory Changes Associated with Obesity through a GPR109A-Dependent Mechanism

1
Department of Genetics, Evolution, Microbiology and Immunology, Institute of Biology, University of Campinas, Campinas 13083007, Brazil
2
Department of Biochemistry, Biomedicine Discovery Institute, Monash University, Melbourne 3800, Australia
3
Department of Clinical Analyses, Federal University of Paraná, Curitiba 80060000, Brazil
4
Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508000, Brazil
5
Interdisciplinary Postgraduate Program in Health Science, Cruzeiro do Sul University, São Paulo 01506000, Brazil
6
Department of Pharmaceutics Sciences, Institute of Environmental Chemistry and Pharmaceutical Sciences, Federal University of São Paulo, Diadema 09972270, Brazil
7
Department of Biological Sciences, Institute of Environmental, Chemical and Pharmaceutical Sciences, Federal University of São Paulo, Diadema 09972270, Brazil
8
Department of Biochemistry, Institute of Chemistry, University of São Paulo, São Paulo 05508000, Brazil
9
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508000, Brazil
10
Butantan Institute, São Paulo 05503900, Brazil
11
Experimental Medicine Research Cluster (EMRC), University of Campinas (UNICAMP), Campinas 13083007, Brazil
12
Obesity and Comorbidities Research Center (OCRC), University of Campinas (UNICAMP), Campinas 13083864, Brazil
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Cells 2020, 9(9), 2007; https://doi.org/10.3390/cells9092007
Received: 6 July 2020 / Revised: 21 August 2020 / Accepted: 24 August 2020 / Published: 1 September 2020
(This article belongs to the Special Issue Molecular Mechanisms in Metabolic Disease)
Obesity 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 obesity. View Full-Text
Keywords: butyrate; microbiota; insulin resistance; dysbiosis butyrate; microbiota; insulin resistance; dysbiosis
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Sato, F.T.; Yap, Y.A.; Crisma, A.R.; Portovedo, M.; Murata, G.M.; Hirabara, S.M.; Ribeiro, W.R.; Marcantonio Ferreira, C.; Cruz, M.M.; Pereira, J.N.B.; Payolla, T.B.; Guima, S.E.S.; Thomas, A.M.; Setubal, J.C.; Alonso-Vale, M.I.C.; Santos, M.F.; Curi, R.; Marino, E.; Vinolo, M.A.R. Tributyrin Attenuates Metabolic and Inflammatory Changes Associated with Obesity through a GPR109A-Dependent Mechanism. Cells 2020, 9, 2007.

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