BACKGROUND: Food polysaccharide 1,3-⊎-D-glucan (OBG) has been shown to alleviate ulcerative colitis (UC) in a mouse model, but the underlying mechanisms remain unclear. Here, we aimed to investigate potential mechanisms involving interactions among gut microbiota, microbial metabolites and host metabolic function.RESULTS: OBG alleviated colonic inflammation, barrier dysfunction and intestinal concentrations of short-chain fatty acids in mice with UC. In addition, the relative abundance of Muribaculaceae, Alistipes, Erysipelatoclostridium and Blautia increased, whereas the abundance of Proteus, Lachnospiraceae and Ruminococcus decreased within the gut microbiota upon OBG treatment. Kyoto Encyclopedia of Genes and Genomes analyses showed that intestinal enzymes altered upon OBG treatment were mainly enriched in sub-pathways of amino acid biosynthesis. Metabolomics analyses showed that L-tryptophan, L-tyrosine, L-phenylalanine and L-alanine increased, which is consistent with the predictive metabolism of gut microbiota. Correlation analysis and interaction networks highlighted gut microbiota (especially Lactobacillus, Parabacteroides, Proteus and Blautia), metabolites (especially L-phenylalanine, L-tryptophan, L-tyrosine and acetic acid) and metabolism (phenylalanine, tyrosine and tryptophan biosynthesis) that may be key targets of OBG.CONCLUSION: OBG is beneficial to the gut microecological balance in mice with colitis, mainly becaue of its impact on the interactions between gut microbes and amino acids metabolism (especially tyrosine and tryptophan metabolism).
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.