# The Gut Commensal Butyricimonas Virosa Modulates Gut Microbiota‐Dependent Thiamine Metabolism and Attenuates Mouse Steatotic Liver Disease

**Authors:** Ningning He, Haoyu Wang, Zizhen Yang, Hui Li, Bei Liu, Kaiwei Chen, Zhinan Wu, Xinnan Zhao, Hewei Liang, Mengmeng Wang, Xiaofang Li, Yiyi Zhong, Haifeng Zhang, Liang Xiao, Karsten Kristiansen, Jixing Peng, Yuanqiang Zou, Shangyong Li

PMC · DOI: 10.1002/advs.202517596 · Advanced Science · 2026-01-20

## TL;DR

A gut bacterium called Butyricimonas virosa, boosted by a prebiotic, helps reduce liver disease by improving thiamine metabolism.

## Contribution

Identifies Butyricimonas virosa as a key gut microbe that mitigates MASLD through thiamine metabolism modulation.

## Key findings

- B. virosa supplementation suppresses MASLD progression in mice fed a high-fat diet.
- B. virosa increases thiamine monophosphate and hepatic thiamine pyrophosphate, enhancing branched-chain amino acid degradation.
- Thiamine metabolism-related genes and serum thiamine levels correlate inversely with MASLD severity in population analysis.

## Abstract

Metabolic dysfunction‐associated steatotic liver disease (MASLD) is a common chronic liver disease. This study investigates the anti‐MASLD effects of dietary prebiotic stachyose (STA) on disease progression identifying Butyricimonas virosa as a key bacterium boosted by STA supplementation. Oral gavage of B. virosa to high fat diet (HFD)‐fed mice significantly suppresses the progression of MASLD and modulates gut microbiota composition. Integration of metagenomic and metabolomic data demonstrates that B. virosa treatment significantly enhances the production of thiamine monophosphate (TMP), as well as its conversion to thiamine and subsequent accumulation in the liver. The accumulation of hepatic thiamine further leads to elevated thiamine pyrophosphate (TPP) concentrations enhancing the activity of branched‐chain α‐keto acid dehydrogenase E1 subunit α (BCKDHA) associated with augmented degradation of branched chain amino acids (BCAAs). Administration of B. virosa compensates via production of gut bacterial‐derived TMP for hepatic TPP deficiency in mice fed a thiamine‐deficient HFD. A population‐based analysis reveals an inverse correlation between plasma thiamine levels, abundances of bacterial genes involved in thiamine synthesis and metabolism, and phenotypes associated with MASLD, suggesting that key genes involved in fecal thiamine metabolism, as well as serum thiamine determination, may potentially serve as biomarkers for the diagnosis of MASLD.

This study reveals that dietary stachyose enriches Butyricimonas virosa, effectively attenuating metabolic dysfunction‐associated steatotic liver disease (MASLD). Mechanistically, B. virosa enhances gut thiamine monophosphate synthesis, which elevates hepatic thiamine pyrophosphate levels. This metabolic restoration promotes branched‐chain amino acid degradation to mitigate hepatic steatosis and inflammation, highlighting a promising microbiota‐targeted therapeutic strategy.

## Linked entities

- **Genes:** BCKDHA (branched chain keto acid dehydrogenase E1 subunit alpha) [NCBI Gene 593]
- **Chemicals:** stachyose (PubChem CID 439531), thiamine monophosphate (PubChem CID 10761), thiamine pyrophosphate (PubChem CID 1132), branched-chain amino acids (PubChem CID 9886134)
- **Diseases:** metabolic dysfunction-associated steatotic liver disease (MONDO:0013209), MASLD (MONDO:0013209)
- **Species:** Butyricimonas virosa (taxon 544645), Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Bckdha (branched chain ketoacid dehydrogenase E1, alpha polypeptide) [NCBI Gene 12039] {aka BCKAD, BCKDE1A, E1[a]}
- **Diseases:** MASLD (MESH:D008107)
- **Chemicals:** STA (MESH:C005695), TPP (MESH:D013835), TMP (MESH:D013833), BCAAs (MESH:D000597), fat (MESH:D005223), Thiamine (MESH:D013831)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Butyricimonas virosa (species) [taxon 544645]

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13042768/full.md

## References

66 references — full list in the complete paper: https://tomesphere.com/paper/PMC13042768/full.md

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Source: https://tomesphere.com/paper/PMC13042768