FABP4 regulates inflammation and lipid transport via PPARγ signaling pathway in goose primary hepatocytes.

Unlike human nonalcoholic fatty liver disease, fatty liver in geese do not induce inflammation even under severe steatosis, making it a unique model for studying hepatic lipid accumulation. Fatty acid-binding protein 4 (FABP4) is known to regulate lipid metabolism and inflammation, but its role in goose fatty liver formation remains unclear. In this study, primary hepatocytes were successfully isolated from Xupu goose and used to investigate the function of FABP4. The results showed that FABP4 overexpression significantly suppressed the mRNA levels of TNF, IL1, IL6, and ApoB (P < 0.05), while FABP4 knockdown upregulated the expression of IL6, ApoB, CD36, and FABP5 (P < 0.05). Transcriptome sequencing analysis revealed that differentially expressed genes mainly enriched in immune response and cytokine-cytokine receptor interaction pathways. Furthermore, treatment with the PPARγ inhibitor partially reversed the suppression of ApoB, IL1, and IL6 induced by FABP4 overexpression, indicating that FABP4 functions downstream of PPARγ. In conclusion, FABP4 selectively suppresses inflammatory cytokines and ApoB expression via the PPARγ signaling pathway in goose primary hepatocytes. This study provides novel evidence in geese for a regulatory relationship between FABP4 and ApoB, offering new insights into the protective mechanisms underlying goose fatty liver formation.