Inflammatory bowel disease (IBD) is a chronic relapsing-remitting systemic disease of the gastrointestinal tract, characterized by an inflammatory process. Gut mycobiota community dysbiosis has been reported that is closely related to the development of IBD. Our previous findings indicated that polyphenol of the inner shell (BPIS) from foxtail millet bran could restore the gut microbiome and inhibit the progress of CRC. In the present study, we studied the anti-inflammatory potential of BPIS in the dextran sodium sulfate (DSS)-induced mouse colitis model. Data suggested that BPIS alleviated experimental colitis by restoring body weight, colonic length and protecting the epithelial architecture from damage by DSS. Moreover, we found that BPIS strengthened the gut barrier function and inhibited the activation of Wnt1/β-catenin pathway. Gene sequence analysis indicated that BPIS remodeled the overall structure of the gut mycobiota from colitis mice toward that of the normal counterparts, including one phylum and nine genera. Interestingly, BPIS significantly increased the abundance of Aspergillus ruber (P < 0.05). It further verified that BPIS significantly promoted the growth of Aspergillus ruber in vitro. Collectively, BPIS has great potential to develop into an effective against IBD drug.

Metabolic syndrome (MetS) is a chronic disease associated with the disturbance of gut microbiota homeostasis. Metabolites derived from gut microbes play essential roles in MetS prevention and therapy. Here, we focused on the inhibitory effect of the extract of millet bran protein (EMBP) on a high-fat diet (HFD)-induced MetS, aiming to identify gut microbiota and their metabolites that involve in the anti-MetS activity of EMBP.

The obesity, chronic inflammation, insulin resistance in MetS mouse models were abolished after EMBP treatment. The protective mechanism of EMBP against HFD-induced MetS may depend on improved gut barrier function. Using microbiome analysis, we found that EMBP supplementation improved gut microbiome dysbiosis in MetS mice, specifically upregulating Bacteroides acidifaciens. The fecal microbiota transplantation (FMT) also demonstrates this phenomenon. In addition, metabolomic analysis showed that EMBP mediates metabolic profiling reprogramming in MetS mice. Notably, a microbiota-derived metabolite, gamma-aminobutyric acid (GABA), is enriched by EMBP. In addition, exogenous GABA treatment produced a similar protective effect to EMBP by improving NRF2-dependent gut barrier function to protect HFD-induced MetS.

The results suggest that EMBP suppress host MetS by remodeling of gut microbiota as an effective candidate for next-generation medicine food dual purpose dietary supplement to intervene in MetS.