Fig. 8: Proposed mechanisms underlying the anti-MAFLD effect of inulin mediated by M. funiformis CML154. | npj Biofilms and Microbiomes

Fig. 8: Proposed mechanisms underlying the anti-MAFLD effect of inulin mediated by M. funiformis CML154.

From: Inulin-enriched Megamonas funiformis ameliorates metabolic dysfunction-associated fatty liver disease by producing propionic acid

Fig. 8

Dietary inulin modulates the gut microbiota by promoting the growth of M. funiformis CML154. Propionic acid produced by M. funiformis CML154 enters liver through the hepatic portal vein, where it activates APN, which in turn is responsible for activating AMPK and PPARα pathways via binding to its receptors AdipoR1 and AdipoR2. The activation of PPARα together with ACOX1 participates in regulating lipid oxidation. Simultaneously, activated AMPK inhibits hepatic lipogenesis, enhances fatty acid oxidation, and improves hepatic mitochondrial function through regulating downstream target genes.

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