Fatty Acid-Binding Protein 3 (FABP3)-Mediated Abdominal Fat Deposition in Broilers via the PPAR Signaling Pathway
- 1College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China
Abstract
Excessive deposition of abdominal fat in broilers compromises feed efficiency, carcass yield, processing efficiency, and inflates production costs. Because this trait is governed by multi-tissue crosstalk coupling hepatic lipid synthesis to adipose lipid storage, its coordinated regulation has seldom been addressed. We combined three abdominal fat transcriptomic datasets (GSE42980, GSE49121, GSE104039) with one hepatic dataset (GSE104038), obtaining 2520 meta-differentially expressed genes (meta-DEGs). Functional enrichment revealed a prominent enrichment of lipid-metabolism terms, including peroxisome proliferator-activated receptor (PPAR) signaling. Fatty acid-binding protein 3 (FABP3) appeared repeatedly within the Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene set enrichment analysis (GSEA) lipid-metabolism categories and was therefore taken forward for functional work. Overexpressing FABP3 enhanced proliferation, lipid accumulation and lipogenic marker expression, whereas knockdown reversed these effects. In both adipocytes and hepatocytes, FABP3 raised peroxisome proliferator-activated receptor gamma (PPARγ) and fatty acid-binding protein 4 (FABP4) at mRNA and protein levels. Pharmacological intervention showed that the PPARγ antagonist GW9662 suppressed the pro-lipogenic action of FABP3 overexpression, while the PPARα agonist GW7647 reinstated lipid accumulation in FABP3-silenced cells, indicating a reliance on PPAR-pathway activity. FABP3 therefore drives lipid deposition in adipocytes and hepatocytes via PPAR signaling, offering a framework for how the liver and abdominal adipose tissue jointly govern abdominal fat deposition in broilers.
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BibTeX
@article{yuan2026fatty,
title = {{Fatty Acid-Binding Protein 3 (FABP3)-Mediated Abdominal Fat Deposition in Broilers via the PPAR Signaling Pathway}},
author = {Hui Yuan and Yuxin Zhu and Kaibo Jin and Yuan Liu and Jun Lu and Runxiang Zhang},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27219413},
url = {https://www.mdpi.com/1422-0067/27/21/9413},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Fatty Acid-Binding Protein 3 (FABP3)-Mediated Abdominal Fat Deposition in Broilers via the PPAR Signaling Pathway
AU - Hui Yuan
AU - Yuxin Zhu
AU - Kaibo Jin
AU - Yuan Liu
AU - Jun Lu
AU - Runxiang Zhang
PY - 2026
DA - 2026/10/22
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219413
UR - https://www.mdpi.com/1422-0067/27/21/9413
AB - Excessive deposition of abdominal fat in broilers compromises feed efficiency, carcass yield, processing efficiency, and inflates production costs. Because this trait is governed by multi-tissue crosstalk coupling hepatic lipid synthesis to adipose lipid storage, its coordinated regulation has seldom been addressed. We combined three abdominal fat transcriptomic datasets (GSE42980, GSE49121, GSE104039) with one hepatic dataset (GSE104038), obtaining 2520 meta-differentially expressed genes (meta-DEGs). Functional enrichment revealed a prominent enrichment of lipid-metabolism terms, including peroxisome proliferator-activated receptor (PPAR) signaling. Fatty acid-binding protein 3 (FABP3) appeared repeatedly within the Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene set enrichment analysis (GSEA) lipid-metabolism categories and was therefore taken forward for functional work. Overexpressing FABP3 enhanced proliferation, lipid accumulation and lipogenic marker expression, whereas knockdown reversed these effects. In both adipocytes and hepatocytes, FABP3 raised peroxisome proliferator-activated receptor gamma (PPARγ) and fatty acid-binding protein 4 (FABP4) at mRNA and protein levels. Pharmacological intervention showed that the PPARγ antagonist GW9662 suppressed the pro-lipogenic action of FABP3 overexpression, while the PPARα agonist GW7647 reinstated lipid accumulation in FABP3-silenced cells, indicating a reliance on PPAR-pathway activity. FABP3 therefore drives lipid deposition in adipocytes and hepatocytes via PPAR signaling, offering a framework for how the liver and abdominal adipose tissue jointly govern abdominal fat deposition in broilers.
SN - 1422-0067
ER -