Fatty Acid-Binding Protein 3 (FABP3)-Mediated Abdominal Fat Deposition in Broilers via the PPAR Signaling Pathway

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.