Obesity is a metabolic disease associated with gut microbiota and low-grade chronic inflammation. Tremella fuciformis is a medicinal and edible fungus; polysaccharide (TP) is the main active component, which has a variety of biological activities, such as hypoglycemic and hypolipidemic. However, the anti-obesity effects and potential mechanisms of TP have never been reported. This study was conducted to elucidate the inhibitory effect of TP on high-fat diet (HFD)-induced obesity in mice. Mice were split into five groups: normal chow diet (NCD) group, NCD_TP_H group, HFD group, HFD_TP_L group and HFD_TP_H group. Our study showed that TP inhibited high-fat diet-induced weight gain and fat accumulation in mice and reduced blood glucose, hyperlipidemia and inflammation. TP also improved gut microbiota disorders by reducing the Firmicutes/Bacteroidetes ratio and modulating the relative abundance of specific gut microbiota. We also found that the anti-obesity and gut microbiota-modulating effects of TP could be transferred to HFD-fed mice via faecal microbiota transplantation (FMT), confirming that the gut microbiota was one of the targets of TP for obesity inhibition. Further studies showed that TP increased the production of short-chain fatty acids and the secretion of intestinal hormones. Our studies showed that TP inhibited obesity by modulating inflammation and the microbe-gut-brain axis, providing a rationale for developing TP to treat obesity and its complications.

It has been shown that Tibetan tea (TT) inhibits obesity and controls lipid metabolism. The fundamental processes by which TT prevents obesity are yet entirely unknown. Consequently, this research aimed to ascertain if TT may prevent obesity by modifying the gut flora. Our research demonstrated that TT prevented mice from gaining weight and accumulating fat due to the high‐fat diet (HFD), decreased levels of blood total cholesterol (TC), triglycerides (TG), and low‐density lipoprotein cholesterol (LDL‐C), and raised levels of high‐density lipoprotein cholesterol (HDL‐C). Adipogenesis‐related genes such as acetyl‐Coenzyme A carboxylase 1 (ACC1, LOC107476), fatty acid synthase (Fas, LOC14104), sterol regulatory element‐binding protein‐1c (SREBP‐1c, LOC20787), CCAAT/enhancer‐binding protein α (C/EBPα, LOC12606), stearoyl‐CoA desaturase 1 (SCD1, LOC20249), and peroxisome proliferator‐activated receptor γ (PPARγ, LOC19016) had their expression downregulated by lowering the Firmicutes/Bacteroidetes (F/B) ratio and controlling the number of certain gut bacteria. TT also alleviated HFD‐induced abnormalities of the gut microbiota. The Muribaculaceae, Lachnospiraceae NK4A136_group, Alistipes, and Odoribacter families were identified as the major beneficial gut microorganisms using Spearman's correlation analysis. Fecal microbiota transplantation (FMT) demonstrated that TT's anti‐obesity and gut microbiota‐modulating benefits might be transmitted to mice on an HFD, demonstrating that one of TT's targets for preventing obesity is the gut microbiota. TT also increased the amount of short‐chain fatty acids (SCFAs) in the feces, including acetic, propionic, and butyric acids. These results indicate the possible development of TT as a prebiotic to combat obesity and associated disorders. These results suggest that TT may act as a prebiotic against obesity and its associated diseases.