# Fecal microbiota transplantation improves functional constipation through the gut microbiome–bile acid–receptor axis

**Authors:** Dongxu Wen, Shuzhen Liu, Yukun Wu, Haixuan Zhang, Kun Zhang

PMC · DOI: 10.3389/fmed.2026.1751593 · Frontiers in Medicine · 2026-02-09

## TL;DR

Fecal microbiota transplantation helps with constipation by changing gut bacteria and bile acid levels, which affects gut movement and improves symptoms.

## Contribution

This paper identifies the gut microbiome–bile acid–receptor axis as a novel mechanism through which FMT improves functional constipation.

## Key findings

- FMT improves bowel movements and stool consistency in patients with functional constipation.
- FMT modulates bile acid profiles and activates FXR and TGR5 signaling pathways to enhance intestinal function.
- Microbial diversity restoration and bile acid metabolism are key to FMT's therapeutic effects.

## Abstract

Functional Constipation (FC) is a prevalent gastrointestinal motility disorder worldwide that markedly impairs patients’ quality of life, yet the currently available treatment options often show limited efficacy. In recent years, research has gradually revealed the critical role of the gut microbiota and bile acid metabolism in the pathogenesis of FC. Fecal Microbiota Transplantation (FMT), which restores the intestinal microecological balance by transferring gut microbiota from healthy donors, has demonstrated clinical efficacy in promoting bowel movements, improving stool consistency, and enhancing patients’ quality of life. However, its underlying mechanisms remain incompletely understood. Current evidence indicates that FMT restores microbial diversity, increases beneficial taxa, and partially reconstructs the bile acids (BAs) profile, thereby modulating Farnesoid X Receptor (FXR) and Takeda G Protein–Coupled Receptor 5 (TGR5) mediated signaling pathways to enhance intestinal secretion and alleviate constipation-related symptoms. The resulting microbiota–bile acid–receptor pathway elucidates the mechanistic link between microbial remodeling and host gastrointestinal motility, thereby offering theoretical support for the therapeutic application of FMT in functional constipation.

## Full-text entities

- **Genes:** NR1H4 (nuclear receptor subfamily 1 group H member 4) [NCBI Gene 9971] {aka BAR, FXR, HRR-1, HRR1, PFIC5, RIP14}, GPBAR1 (G protein-coupled bile acid receptor 1) [NCBI Gene 151306] {aka BG37, GPCR19, GPR131, M-BAR, TGR5}, CYP7A1 (cytochrome P450 family 7 subfamily A member 1) [NCBI Gene 1581] {aka CP7A, CYP7, CYPVII}, Gcg (glucagon) [NCBI Gene 14526] {aka GLP-1, Glu, PPG}
- **Diseases:** weight (MESH:D015431), gastrointestinal motility disorder (MESH:D005767), Functional Constipation (MESH:D003248), type 2 diabetes (MESH:D003924), depression (MESH:D003866), PD (MESH:D010300), inflammation (MESH:D007249), loss (MESH:D016388), Anxiety (MESH:D001007), obese (MESH:D009765)
- **Chemicals:** INT-777 (MESH:C545501), omega-MCA (-), levodopa (MESH:D007980), BAs (MESH:D001647), LCA (MESH:D008095), CDCA (MESH:D002635), Butyrate (MESH:D002087), obeticholic acid (MESH:C464660), UDCA (MESH:D014580), 5-HT (MESH:D012701), Bas (MESH:D001464), SCFA (MESH:D005232), omega-muricholic acid (MESH:C004821), DCA (MESH:D003840), CA (MESH:D019826), water (MESH:D014867), cAMP (MESH:D000242), chloride (MESH:D002712), INT-767 (MESH:C000602622)
- **Species:** Faecalibacterium prausnitzii (species) [taxon 853], Homo sapiens (human, species) [taxon 9606], Collinsella (genus) [taxon 102106], Bacteroides (genus) [taxon 816], Bacillota (clostridial firmicutes, phylum) [taxon 1239], gut metagenome (species) [taxon 749906], Mus musculus (house mouse, species) [taxon 10090], [Clostridium] scindens (species) [taxon 29347], Actinomycetota (actinobacteria, phylum) [taxon 201174], Roseburia (genus) [taxon 841]

## Full text

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## Figures

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## References

69 references — full list in the complete paper: https://tomesphere.com/paper/PMC12927072/full.md

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Source: https://tomesphere.com/paper/PMC12927072