Cell reportsMar 25, 2014

Probiotics change gut bacteria and increase liver bile acid production by lowering a specific feedback signal in mice

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Mar 28, 2026

Abstract

Gut microbiota modulation by VSL#3 probiotics enhances bile acid deconjugation and fecal excretion in mice.

Probiotic treatment alters bile acid absorption in the ileum.
The enterohepatic farnesoid X receptor-fibroblast growth factor 15 (FXR-FGF15) pathway is repressed following probiotic administration.
Increased hepatic bile acid synthesis occurs in response to changes induced by the probiotics.
Administering an FXR agonist normalizes fecal bile acid levels in mice treated with probiotics.
Deficiency in FXR and FGF15 negates the probiotic effects on bile acid metabolism.

Simplified

Gut microbiota influences host health status by providing trophic, protective, and metabolic functions, including bile acid (BA) biotransformation. Microbial imprinting on BA signature modifies pool size and hydrophobicity, thus contributing to BA enterohepatic circulation. Microbiota-targeted therapies are now emerging as effective strategies for preventing and/or treating gut-related diseases. Here, we show that gut microbiota modulation induced by VSL#3 probiotics enhances BA deconjugation and fecal excretion in mice. These events are associated with changes in ileal BA absorption, repression of the enterohepatic farnesoid X receptor-fibroblast growth factor 15 (FXR-FGF15) axis, and increased hepatic BA neosynthesis. Treatment with a FXR agonist normalized fecal BA levels in probiotic-administered mice, whereas probiotic-induced alterations in BA metabolism are abolished upon FXR and FGF15 deficiency. Our data provide clear in vivo evidence that VSL#3 probiotics promote ileal BA deconjugation with subsequent fecal BA excretion and induce hepatic BA neosynthesis via downregulation of the gut-liver FXR-FGF15 axis.

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Probiotics change gut bacteria and increase liver bile acid production by lowering a specific feedback signal in mice

Abstract

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