Sucrose-preferring gut microbes prevent host obesity by producing exopolysaccharides

Commensal bacteria affect host health by producing various metabolites
from dietary carbohydrates via bacterial glycometabolism; however, the
underlying mechanism of action remains unclear. Here, we identified
Streptococcus salivarius as a unique anti-obesity commensal bacterium. We
found that S. salivarius may prevent host obesity caused by excess sucrose
intake via the exopolysaccharide (EPS)-short-chain fatty acid
(SCFA)-carbohydrate metabolic axis. Healthy human donor-derived S.
salivarius produced high EPS levels from sucrose but not from other
sugars. S. salivarius abundance was significantly decreased in human
donors with obesity, and the EPS-SCFA bacterial carbohydrate metabolic
process was attenuated. Our findings reveal an important mechanism by
which host–commensal interactions in glycometabolism affect energy
regulation, suggesting an approach for preventing lifestyle-related
diseases via prebiotics and probiotics by targeting bacteria and EPS
metabolites.

共生细菌通过自身糖代谢（glycometabolism）利用膳食碳水化合物产生多种代谢物，进而影响宿主健康，但其具体作用机制仍未明确。本研究鉴定出唾液链球菌（Streptococcus salivarius）是一种独特的抗肥胖共生菌。研究发现，唾液链球菌可通过胞外多糖（exopolysaccharide, EPS）-短链脂肪酸（short-chain fatty acid, SCFA）-碳水化合物代谢轴，预防过量蔗糖摄入引发的宿主肥胖。源自健康人类供体的唾液链球菌可利用蔗糖高效合成胞外多糖，而无法以其他糖类完成该代谢过程。肥胖人类供体体内的唾液链球菌丰度显著降低，且其介导的EPS-SCFA细菌糖代谢过程也被削弱。本研究揭示了糖代谢过程中宿主与共生菌的互作调控能量稳态的重要机制，提示可通过靶向细菌与胞外多糖代谢物，借助益生元（prebiotics）与益生菌（probiotics）手段预防生活方式相关疾病。