# Limosilactobacillus reuteri ATG-F4 Improves the Muscle Strength and Muscle Mass of Mice with Immobilization-Induced Muscular Atrophy

**Authors:** Daeyoung Lee, Young-Sil Lee, Gun-Seok Park, Juyi Park, Seung-Hyun Ko, You-Kyung Lee, Do Yeun Jeong, Yong Hyun Lee, Jihee Kang

PMC · DOI: 10.4014/jmb.2506.06004 · Journal of Microbiology and Biotechnology · 2025-10-15

## TL;DR

A gut bacterium called Limosilactobacillus reuteri ATG-F4 helps prevent muscle loss in mice by boosting muscle strength and protein synthesis.

## Contribution

This study is the first to demonstrate that ATG-F4 prevents muscle atrophy through gut-muscle axis modulation and mTOR signaling activation.

## Key findings

- ATG-F4 preserved muscle mass and improved grip strength in immobilized mice.
- ATG-F4 activated mTOR signaling and suppressed MuRF1, a key atrophy factor.
- ATG-F4 altered gut microbiota and increased serum levels of butyrate and acetate.

## Abstract

Probiotics offer a promising avenue for combating muscle atrophy, which is a debilitating condition associated with muscle disuse, aging, and disease. This study investigated the anti-atrophic potential of Limosilactobacillus reuteri ATG-F4, a human gut-derived bacterium, in a mouse model of staple-induced immobilization. ATG-F4 administration significantly preserved muscle mass and improved grip strength and endurance. Mechanistically, ATG-F4 activated mTOR signaling and promoted protein synthesis. Additionally, ATG-F4 downregulated MuRF1, a key atrophy factor. Furthermore, ATG-F4 administration significantly altered the composition of the gut microbiota, favoring the presence of the Muribaculaceae family and decreasing the abundance of Lachnospiraceae and Lactobacillaceae. Administration of ATG-F4 increased serum levels of the short-chain fatty acids (SCFAs) butyrate and acetate. SCFAs, which are produced by bacterial fermentation in the gut, possess anti-inflammatory and beneficial muscle properties and exert several effects on host metabolism and the immune system. Therefore, we suggest that the potential mechanism underlying the anti-atrophic effects of ATG-F4 on muscles involves the enhancement of muscle protein synthesis, suppression of protein degradation, and modulation of the gut-muscle axis. These findings highlight the potential of ATG-F4 as a prophylactic or therapeutic agent for the treatment of muscle atrophy.

## Linked entities

- **Genes:** TRIM63 (tripartite motif containing 63) [NCBI Gene 84676]
- **Proteins:** MTOR (mechanistic target of rapamycin kinase)
- **Chemicals:** butyrate (PubChem CID 104775), acetate (PubChem CID 175)
- **Species:** Limosilactobacillus reuteri (taxon 1598), Muribaculaceae (taxon 2005473), Lachnospiraceae (taxon 186803), Lactobacillaceae (taxon 33958)

## Full-text entities

- **Genes:** Trim63 (tripartite motif-containing 63) [NCBI Gene 433766] {aka MuRF1, RF1, Rnf28}, Mtor (mechanistic target of rapamycin kinase) [NCBI Gene 56717] {aka 2610315D21Rik, FRAP, FRAP2, Frap1, RAFT1, RAPT1}
- **Diseases:** inflammatory (MESH:D007249), Muscular Atrophy (MESH:D009133), atrophic (MESH:D020966), atrophy (MESH:D001284)
- **Chemicals:** acetate (MESH:D000085), ATG-F4 (-), butyrate (MESH:D002087), SCFAs (MESH:D005232)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12549228/full.md

## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12549228/full.md

## References

65 references — full list in the complete paper: https://tomesphere.com/paper/PMC12549228/full.md

---
Source: https://tomesphere.com/paper/PMC12549228