Inulin-enriched Megamonas funiformis ameliorates metabolic dysfunction-associated fatty liver disease by producing propionic acid.
Xinyue YangMeihong ZhangYan LiuFuxiao WeiXin LiYuqing FengXiaolu JinDan LiuYuming GuoYongfei HuPublished in: NPJ biofilms and microbiomes (2023)
Accumulated evidence supports the beneficial role of inulin in alleviating metabolic dysfunction-associated fatty liver disease (MAFLD) by modulating gut microbiota. However, the underlying mechanisms are not fully understood. Here we used high-fat diet (HFD)-induced laying hen model of MAFLD to investigate the effect of inulin on ameliorating MAFLD and found that the inulin-enriched Megamonas genus was inversely correlated with hepatic steatosis-related parameters. Oral administration of a newly isolated commensal bacterium by culturomics, M. funiformis CML154, to HFD-fed hens and mice ameliorated MAFLD, changed liver gene expression profiles, and increased intestinal propionate concentration. Further evidence demonstrated that the anti-MAFLD effect of M. funiformis CML154 is attributed to propionate-mediated activation of the APN-AMPK-PPARα signaling pathway, thereby inhibiting fatty acid de novo synthesis and promoting β-oxidation. These findings establish the causal relationships among inulin, M. funiformis, and MAFLD, and suggest that M. funiformis CML154 is a probiotic candidate for preventative or therapeutic intervention of MAFLD.
Keyphrases
- high fat diet
- signaling pathway
- insulin resistance
- fatty acid
- adipose tissue
- randomized controlled trial
- oxidative stress
- skeletal muscle
- high fat diet induced
- chronic myeloid leukemia
- heat stress
- genome wide
- diabetic rats
- pi k akt
- metabolic syndrome
- gene expression
- induced apoptosis
- high glucose
- hydrogen peroxide
- genome wide identification
- electron transfer