Pu-erh tea, a traditional Chinese beverage, performs an anti-obesity function, but the correlation between its components and efficacy remains unknown. Here, we screened two Pu-erh teas with significant anti-obesity efficacies from 11 teas. In vitro experiments revealed that lipid accumulation in L02 cells and lipid synthesis in 3T3-L1 cells were significantly better inhibited by Tea-B than Tea-A. Further in vivo experiments using model mice revealed that the differences in chemical components generated two pathways in the anti-obesity efficacy and mechanism of Pu-erh teas. Tea-A changes the histomorphology of brown adipose tissue (BAT) and increases the abundance of Coriobacteriaceae_UCG_002 and cyclic AMP in guts through high chemical contents of cyclopentasiloxane, decamethyl, tridecane and 1,2,3-trimethoxybenzene, eventually increasing BAT activation and fat browning gene expression; the high content of hexadecane and 1,2-dimethoxy-benzene in Tea-B reduces white adipose tissue (WAT) accumulation and the process of fatty liver, increases the abundance of Odoribacter and sphinganine 1-phosphate, inhibits the expression of lipid synthesis and transport genes. These mechanistic findings on the association of the representative bioactive components in Pu-erh teas with the anti-obesity phenotypes, gut microbes, gut metabolite structure and anti-obesity pathways, which were obtained for the first time, provide foundations for developing functional Pu-erh tea.

Ulcerative colitis (UC) is a chronic systematic inflammation disorder with increasing incidence, unknown pathogenesis, limited drug treatment, and abundant medical expenses. Dietary intake, as a daily indispensable environment factor, is closely related to UC pathogenesis and prevention. The underlying interactions between dietary intake and UC progression are implicated with the modulation of gut microbiome as well as microbial metabolites, suggesting the complex and systematic characteristics of UC. However, the triangular relationships with dietary intake, gut microbiota homeostasis, and UC have not been well summarized so far. Here we review the recent studies of dietary intake on the regulation of gut microbiome homeostasis as well as modulation of UC progression. These findings suggest that varieties in dietary patterns result in the production of diverse microbial fermentation metabolites, which contribute to gut microbiome homeostasis through multiple manipulations including immune modulation, inflammation restriction as well as epithelial barrier maintenance, thus finally determine the fate of UC progression and give implications for functional food development for prevention and treatment of UC patients.