Lipidomic and Transcriptomic Reveals Variations in Lipid Deposition During Goose Fatty Liver Formation

Goose foie gras production requires force-feeding with high-energy feed, disrupting hepatic lipid homeostasis and causing excessive lipid accumulation. To investigate the formation mechanism, we collected liver samples from Landes geese at pre-force-feeding (D0), mid-force-feeding (D16), and terminal-force-feeding (D25) stages. Overfeeding shifted liver color from reddish-brown to yellow, significantly increasing size and weight. Histological analysis revealed pronounced lipid droplet accumulation in hepatocytes. Biochemical analysis indicated force-feeding groups (D16, D25) exhibited continuous and significant decreases in liver moisture, crude ash, and crude protein content compared to D0, while crude fat increased substantially. Integrated transcriptomic and lipidomic analyses identified 497 differentially expressed genes (DEGs) and 368 differential lipid molecules (DLMs) between D16 and D0, and 303 DEGs and 172 DLMs between D25 and D16. KEGG enrichment highlighted four pathways associated with fatty liver formation: glycerolipid metabolism, adipocytokine signaling pathway, ErbB signaling pathway, and MAPK signaling pathway. Within these, key genes (DGAT2, LIPG, LPL, LPIN1, NFKBIA, SLC2A1, AREG, DUSP1, DUSP10, PPARGC1A, NR4A1, PAK5) potentially regulate critical lipid metabolites (1-acyl-sn-glycerol-3-phosphate, 1,2-diacyl-sn-glycerol-3-phosphate, diglyceride, triacylglycerol). These genes and metabolites likely play a dominant role in the development of goose fatty liver, collectively promoting hepatic triacylglycerol accumulation and the progression of goose fatty liver.