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Abstract Background & Aims: Tributyrin (TB) is a stable form of butyrate. Butyrate is a major short-chain fatty acid (SCFA) produced by bacterial fermentation of dietary fiber in the colon by commensal bacteria. Studies have shown that butyrate maintains the differentiated state of the colon and is a potent anti-inflammatory and anti-cancer agent. In addition, butyrate stimulates the host’s innate immune system. We have established that butyrate stimulates ZBP gene expression and serotonin (5HT) production, which subsequently stimulates the release of antimicrobial peptides during the infection by Salmonella typhimurium. We investigated whether tributyrate modulates gut homeostasis and cellular functions during inflammation-driven colitis. Method: We used dextran sulfate sodium (DSS)-induced colitis mice model using C57/B6J mice. 10 male group of mice received DSS in water and were given a normal rodent chaw diet without tributyrin supplement. 10 male group of mice received DSS in water and were given a normal rodent chaw diet with tributyrin supplement. Result: Tributyrin prevented weight loss which was significantly observed in mice treated with DSS without tributyrin in diet. Additionally, tributyrin prevented colon shortening and significantly suppresses inflammation. Mice treated with DSS alone exhibited significant clinical scores, whereas mice receiving DSS with Tributyrin were trending towards recovery after day 5. Furthermore, histological studies revealed that tributyrin significantly impeded the development of inflammation, epithelial damage and hyperplasia in DSS-induced mice model. Conclusion: These results indicated that tributyrin mitigates the inflammatory effects of DSS on mucosal epithelial tissue, presumably due in part to 5HT production in response to butyrate.
Brantley et al. (Fri,) studied this question.