Propionate–producing bacteria, Acidipropionibacterium acidipropionici, prevents metabolic dysregulation via GPR41 signaling in high-fat diet-induced obese mice

Abstract

Obesity is a major healthcare problem worldwide and is induced by excess energy intake, resulting in gut microbial composition and microbial diversity changes. Through fermentation of dietary fibers, short-chain fatty acids (SCFAs) act as host energy sources and signaling molecules via G protein-coupled receptors such as GPR41. Acidipropionibacterium acidipropionici is widely used in many applications; however, in vivo studies on the effect of A. acidipropionici on propionate production and the regulation of energy homeostasis are unclear. Therefore, this study aimed to investigate the beneficial metabolic effects of A. acidipropionici by focusing on GPR41 signaling in a high-fat diet (HFD)-induced obesity mouse model. Here, we demonstrated that A. acidipropionici OB7439 (OB7439) improved host metabolism in HFD-induced obesity in mice. The intake of OB7439 improved metabolism in HFD-induced obese mice by increasing propionate production, regulating glucose tolerance, and inhibiting hepatic inflammation via GPR41 signaling. Our findings shed light on the potential of using OB7439 as an SCFA producer for the prevention and treatment of metabolic disorders. Based on these results, A. acidipropionici may serve as a potential therapeutic bacteria that inhibits obesity and modulates the gut microbial community.