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Scope This study examines the beneficial effects of Goji berry against spontaneous colitis and its prebiotic role in IL‐10‐deficient mice. Methods IL‐10‐deficient mice are assigned to a standard rodent diet (control) or a control diet supplemented with Goji (1% of dry feed weight) for 10 weeks, at which point colonic tissues and fecal contents are collected. Results Goji supplementation decreases colonic pathobiological scores and mRNA expression of Il17a and Tgfb1, while it enhances Muc1 expression and fecal IgA content. Illumina MiSeq sequencing reveals that Goji supplementation increases Actinobacteria phylum, resulting in a bloom of Bifidobacteria in gut microbiota. Additionally, dietary Goji promotes butyrate‐producing bacteria including Lachnospiraceae‐Ruminococcaceae family and Roseburia spp. under Clostridium cluster XIVa. Furthermore, butyrate‐producers Clostridium leptum and its dominant constituent Fecalibacterium prazusnitzii are markedly increased in the Goji group. Moreover, the gene‐encoding butyryl‐coenzyme A CoA transferase, a key enzyme responsible for butyrate synthesis in butyrate‐producing bacteria, is increased sixfold in the fecal samples of Goji group associated with increased fecal butyrate content. Conclusion Data collectively show that dietary Goji results in the blooming of Bifidobacteria and butyrate‐producing bacteria. These bacteria may cross‐feed each other, conferring preventative effects against colitis in IL‐10‐deficient mice.

Defect in intestinal epithelial structure is a critical etiological factor of several intestinal diseases such as inflammatory bowel disease. The objective of this study was to evaluate the effect of grape seed extract (GSE), which contains a mixture of polyphenols, on ileal mucosal structure and inflammation in interleukin (IL)-10-deficient mice, a common model for studying inflammatory bowel disease. Wild-type and IL-10-deficient mice were fed GSE at 0 or 1% (based on dry feed weight) for 16 weeks. GSE supplementation decreased crypt depth and increased (P < 0.05) the ratio of villus/crypt length in the terminal ileum. Consistently, the dietary GSE decreased (P < 0.05) proliferation and enhanced (P < 0.05) differentiation of epithelial cells. These changes in gut epithelium were associated with the suppression of nuclear factor kappa-light-chain-enhancer of activated B-cell (NF-κB) signaling. Furthermore, compared with WT mice, IL-10 deletion promoted beclin-1 and AMPK expression, both of which were decreased to normal by GSE supplementation. These changes were associated with alterations in epithelial barrier function as indicated by reduced pore forming claudin-2 protein expression and increased barrier forming claudin-1 protein expression in the ileum of GSE supplemented mice. In summary, our data indicates that GSE exerts protective effects to the ileal epithelial structure in IL-10-deficient mice possibly through the suppression of inflammatory response.

Dietary RB attenuated adipocyte hypertrophy and inflammation of WAT in HFD-mice and improves insulin sensitivity and beige adipogenesis, which is associated with increased FNDC5/irisin content and activation of AMPK/Sirt1 pathway. RB supplementation provides a promising strategy to prevent diet-induced obesity.

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