# Mechanisms of gut microbiota in host fat deposition: metabolites, signaling pathways, and translational applications

**Authors:** Sha Liu

PMC · DOI: 10.3389/fmicb.2025.1675155 · Frontiers in Microbiology · 2025-12-18

## TL;DR

This review explores how gut microbes influence fat storage in the body through various metabolites and signaling pathways, and discusses potential interventions for obesity.

## Contribution

The paper systematically reviews the mechanisms of gut microbiota in host fat deposition and translational applications for obesity control.

## Key findings

- Gut microbial metabolites like SCFAs and TMAO regulate host lipid metabolism and epigenetics.
- Signaling pathways such as Wnt/β-catenin and PPARγ are involved in gut microbiota-mediated fat deposition.
- Interventions like probiotics and fecal transplantation show potential in obesity control and animal production.

## Abstract

Obesity and metabolic diseases are global health challenges, with gut microbiota playing a critical role in host fat deposition through symbiotic interactions. In recent years, the gut microbiota, as an important factor regulating fat deposition, has received widespread attention. Numerous studies have confirmed that gut microbes influence host fat accumulation by regulating energy metabolism, inflammatory response, and gut barrier function. In this review, we summarized the key roles of gut microbial metabolites, including short-chain fatty acids (SCFAs), bile acids, tryptophan metabolites, lipopolysaccharides (LPS), branched-chain amino acids (BCAAs), and trimethylamine N-oxide (TMAO) in host epigenetic regulation and lipid metabolism, and explored their regulatory mechanisms through mediated signaling pathways, including Wnt/β-catenin signaling pathway, transforming growth factor beta/SMAD3 pathway (TGF-β/SMAD3), peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein alpha (C/EBPα), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). In terms of translational applications, we described the research progress and application potentials of intervention strategies, such as probiotics, prebiotics, synbiotics, postbiotics, and fecal transplantation in obesity control and animal production. Finally, we proposed the current bottlenecks and translational challenges in obesity control by precision nutrition and microecological intervention, and look forward to future directions. This review provides a theoretical basis for the in-depth understanding of the interactions between gut microbiota and host metabolism, and serves as a reference for the prevention and control of metabolic diseases by developing nutritional intervention strategies for animals.

## Linked entities

- **Chemicals:** branched-chain amino acids (PubChem CID 9886134), trimethylamine N-oxide (PubChem CID 1145)
- **Diseases:** obesity (MONDO:0011122)

## Full-text entities

- **Genes:** PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468] {aka CIMT1, FPLD3, GLM1, NR1C3, PPARG1, PPARG2}, CEBPA (CCAAT enhancer binding protein alpha) [NCBI Gene 1050] {aka C/EBP-alpha, CEBP}, SMAD3 (SMAD family member 3) [NCBI Gene 4088] {aka HSPC193, HsT17436, JV15-2, LDS1C, LDS3, MADH3}, CTNNB1 (catenin beta 1) [NCBI Gene 1499] {aka CTNNB, EVR7, MRD19, NEDSDV, armadillo}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}
- **Diseases:** Obesity (MESH:D009765), metabolic diseases (MESH:D008659), inflammatory (MESH:D007249)
- **Chemicals:** BCAAs (MESH:D000597), TMAO (MESH:C005855), tryptophan (MESH:D014364), bile acids (MESH:D001647), SCFAs (MESH:D005232), lipid (MESH:D008055), LPS (MESH:D008070)

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12756826/full.md

## References

216 references — full list in the complete paper: https://tomesphere.com/paper/PMC12756826/full.md

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Source: https://tomesphere.com/paper/PMC12756826