Figure 1.

Energy homeostasis disruption. Abundant nutrient transporters (CD36, Glut2) and various primary fermentation enzymes (α-amylases and amylomaltases) caused by altered gut microbiota in obesity improve the efficiency of digestible energy uptake and promote monosaccharides and SCFAs production. Moreover, the production of SCFAs was also enhanced by the interspecies H2 transfer between bacteria and archaea. The produced monosaccharides and SCFAs in the gut tract can be absorbed by the host. The decrease of Bacteroides and Lactobacillus in obesity leads to the reduction of bile acids, which inactivates TGR5/FXR-mediated signaling pathway in brown adipose tissue, thus reducing uncouple mitochondrial function, thermogenesis, and white adipose tissue browning. Additionally, the presence of SCFAs suppresses FIAF secretion in the intestine, which then inhibits catabolic process, such as β-oxidation. Taken together, the altered gut microbiota in obesity results in more energy uptake and less energy expenditure, which contributes to the progression of obesity. SCFAs, short-chain fatty acids; TGR5, Takeda G protein-coupled receptor 5; FXR, Farnesoid X Receptor; FIAF, fasting-induced adipose factor.