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Page 4 of 14 Cui et al. Microbiome Res Rep. 2025;4:31 https://dx.doi.org/10.20517/mrr.2025.25

Emerging evidence from poultry research underscores the pivotal role of gut microbiota in modulating fat
deposition, largely independent of host genetic background [Table 1]. For instance, specific microbial taxa,
including Methanobrevibacter and Mucispirillum schaedleri, exhibit significant correlations with adipose
[30]
tissue accumulation in chickens . Further investigations reveal that cecal microbiota may modulate
abdominal fat deposition through lipid metabolism pathways. Notably, the relative abundance of
Parabacteroides, Parasutterella, Oscillibacter, and Anaerofustis shows a positive association with fat
deposition, whereas Sphaerochaeta demonstrates an inverse relationship . Additionally, age-dependent
[31]
dynamics in abdominal fat development correlate with shifts in gut microbiota composition. Studies
indicate that Coprobacillus, Shigella, and Butyricicoccus are negatively associated with propionic acid,
[32]
butyric acid, and abdominal fat mass but positively correlate with isobutyric acid levels . In broilers,
dietary succinate (0.4%) reduced abdominal fat deposition by enriching beneficial cecal microbes (e.g.,
Blautia, Sellimonas) and altering amino acid metabolism linked to lipid handling . Coated sodium
[10]
propionate supplementation similarly inhibited fat deposition and reduced feed intake, accompanied by
decreased adipocyte size and modulation of gut microflora, highlighting the role of propionate as a
microbiota-mediated feed additive . Dietary folic acid at 13 mg/kg decreased abdominal fat and increased
[11]
SCFA-producing taxa, suggesting that vitamin-microbiota synergy can fine-tune carcass composition in
broilers . Dietary fiber treatment reduced abdominal fat and altered gut microbiota in yellow-feathered
[33]
broilers fed corncob meal, decreasing Phascolarctobacterium, Rikenellaceae, and Faecalibacterium while
[12]
increasing Akkermansia . Studies utilizing FMT demonstrated that folic acid supplementation mitigates
abdominal adipose accumulation in broilers, a process potentially mediated by gut microbial shifts. LEfSe
analysis identified Lactobacillus, Clostridium, and Dehalobacterium as dominant taxa in the folic acid-
[34]
treated group, suggesting their role in this regulatory mechanism . Furthermore, dietary inclusion of
fermented grape seed meal enhances broiler growth performance while suppressing abdominal fat
[35]
deposition, likely via modulation of intestinal microbial communities . In parallel, phytosterol
supplementation alters gut microbiota composition in broilers, characterized by reduced bacterial alpha
diversity and a marked increase in probiotic populations such as Lactobacillus within intestinal digesta . In
[36]
addition, correlation analysis revealed that many Firmicutes members had a highly positive relationship
with blood lipid levels and fat storage capacity, which might contribute to the lower abdominal fat
phenotype [37-39] . These findings collectively demonstrate that targeted modulation of gut microbiota through
diet or microbial interventions offers a promising strategy for controlling fat accumulation in broilers.

MECHANISMS OF MICROBIOTA-MEDIATED LIPID METABOLISM
SCFAs
SCFAs are produced by microbial fermentation of dietary fibers and serve as pivotal regulators of host lipid
metabolism. SCFAs produced by the gut microbiota are absorbed across the intestinal epithelium and
metabolized into acetyl-CoA via β-oxidation, playing a pivotal role in systemic lipid metabolism,
lipogenesis, gluconeogenesis, and cholesterol synthesis . Additionally, SCFAs function as signaling
[45]
molecules by binding to and activating free fatty acid receptors (FFARs/GPRs), a class of GPCRs. This
activation stimulates the secretion of glucagon-like peptide-1 (GLP-1) and modulates de novo lipogenesis,
[46]
thereby enhancing glucose and lipid metabolism in adipose tissue and the liver . SCFAs participate in the
regulation of multiple signaling pathways associated with lipid metabolism [Figure 1]. On one hand, SCFAs
modulate the transcription of key hepatic enzymes involved in lipid synthesis, such as fatty acid synthase
(FAS) and acetyl-CoA carboxylase (ACC), and activate the uncoupling protein 2 (UCP2)/adenosine
monophosphate-activated protein kinase (AMPK)/ACC signaling pathway, thereby promoting
[47]
mitochondrial fatty acid oxidation . On the other hand, SCFAs upregulate the expression of peroxisome
proliferator-activated receptor γ coactivator-1α (PGC-1α), further activating the AMPK signaling cascade,
which facilitates fatty acid oxidation while concurrently suppressing lipogenesis . SCFAs, the principal
[48]
microbial metabolites derived from colonic dietary fiber fermentation, play a pivotal role in modulating host