Fang Han, Rodrigues E-Lacerda Rodrigo, Barra Nicole G, Kukje Zada Dana, Robin Nazli, Mehra Alina, Schertzer Jonathan D
Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, and Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada, L8N 3Z5.
Endocr Rev. 2025 Jan 10;46(1):60-79. doi: 10.1210/endrev/bnae025.
The gut microbiota influences aspects of metabolic disease, including tissue inflammation, adiposity, blood glucose, insulin, and endocrine control of metabolism. Prebiotics or probiotics are often sought to combat metabolic disease. However, prebiotics lack specificity and can have deleterious bacterial community effects. Probiotics require live bacteria to find a colonization niche sufficient to influence host immunity or metabolism. Postbiotics encompass bacterial-derived components and molecules, which are well-positioned to alter host immunometabolism without relying on colonization efficiency or causing widespread effects on the existing microbiota. Here, we summarize the potential for beneficial and detrimental effects of specific postbiotics related to metabolic disease and the underlying mechanisms of action. Bacterial cell wall components, such as lipopolysaccharides, muropeptides, lipoteichoic acids and flagellin, have context-dependent effects on host metabolism by engaging specific immune responses. Specific types of postbiotics within broad classes of compounds, such as lipopolysaccharides and muropeptides, can have opposing effects on endocrine control of host metabolism, where certain postbiotics are insulin sensitizers and others promote insulin resistance. Bacterial metabolites, such as short-chain fatty acids, bile acids, lactate, glycerol, succinate, ethanolamine, and ethanol, can be substrates for host metabolism. Postbiotics can fuel host metabolic pathways directly or influence endocrine control of metabolism through immunomodulation or mimicking host-derived hormones. The interaction of postbiotics in the host-microbe relationship should be considered during metabolic inflammation and metabolic disease.
肠道微生物群会影响代谢性疾病的多个方面，包括组织炎症、肥胖、血糖、胰岛素以及代谢的内分泌控制。人们常常寻求使用益生元或益生菌来对抗代谢性疾病。然而，益生元缺乏特异性，并且可能对细菌群落产生有害影响。益生菌需要活细菌来找到足以影响宿主免疫或代谢的定植位点。后生元包括细菌衍生的成分和分子，它们在改变宿主免疫代谢方面具有优势，无需依赖定植效率，也不会对现有微生物群产生广泛影响。在这里，我们总结了特定后生元对代谢性疾病有益和有害影响的潜力以及潜在的作用机制。细菌细胞壁成分，如脂多糖、胞壁肽、脂磷壁酸和鞭毛蛋白，通过引发特定的免疫反应，对宿主代谢产生取决于环境的影响。在脂多糖和胞壁肽等大类化合物中的特定类型后生元，可能对宿主代谢的内分泌控制产生相反的影响，其中某些后生元是胰岛素增敏剂，而其他后生元则会促进胰岛素抵抗。细菌代谢产物，如短链脂肪酸、胆汁酸、乳酸、甘油、琥珀酸、乙醇胺和乙醇，可作为宿主代谢的底物。后生元可以直接为宿主代谢途径提供能量，或者通过免疫调节或模拟宿主衍生的激素来影响代谢的内分泌控制。在代谢性炎症和代谢性疾病期间，应考虑后生元在宿主 - 微生物关系中的相互作用。
