Tributyrin attenuates metabolic and inflammatory changes associated with obesity through a GPR109A-dependent mechanism
Sato, Fabio Takeo; Yap, Yu Anne; Crisma, Amanda Rabello; Portovedo, Mariana; Murata, Gilson Masahiro; Hirabara, Sandro Massao; Ribeiro, Willian Rodrigues; Ferreira, Caroline Marcantonio; Cruz, Maysa Mariana; Pereira, Joice Naiara Bertaglia; Payolla, Tanyara Baliani; Guima, Suzana Eiko Sato; Thomas, Andrew Maltez; Setubal, João Carlos; Alonso-Vale, Maria Isabel Cardoso; Santos, Marinilce Fagundes; Curi, Rui ; Marino, Eliana; Vinolo, Marco A. R.
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
butyrate; microbiota; insulin resistance; dysbiosis
Sato 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.
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