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To comprehensively provide insight into goose fatty liver formation, we performed an integrative analysis of the liver transcriptome, lipidome, and amino acid metabolome, as well as peripheral adipose tissue transcriptome analysis using samples collected from the overfed geese and normally fed geese. Transcriptome analysis showed that liver metabolism pathways were mainly enriched in glucolipid metabolism, amino acid metabolism, inflammation response, and cell cycle; peripheral adipose tissue and the liver cooperatively regulated liver lipid accumulation during overfeeding. Liver lipidome patterns obviously changed after overfeeding, and 157 different lipids were yielded. In the liver amino acid metabolome, the level of Lys increased after overfeeding. In summary, this is the first study describing goose fatty liver formation from an integrative analysis of transcriptome, lipidome, and amino acid metabolome, which will provide a whole new dimension to understanding the mechanism of goose fatty liver formation.

To further explore the fructose pro-steatosis mechanism, we performed an integrative analysis of liver transcriptome and lipidome as well as peripheral adipose tissues transcriptome analysis using samples collected from geese overfed with maize flour (control group) and geese overfed with maize flour supplemented with 10% fructose (treatment group). Overfeeding period of the treatment group was significantly shorter than that of the control group (p < 0.05). Dietary supplementation with 10% fructose induced more severe steatosis in goose liver. Compared with the control group, the treatment group had lower in ceramide levels (p < 0.05). The key differentially expressed genes (DEGs) (control group vs. treatment group) involved in liver fatty acid biosynthesis and steroid biosynthesis were downregulated. The conjoint analysis between DEGs and different lipids showed that fatty acid biosynthesis and steroid biosynthesis were the highest impact score pathways. In conclusion, fructose expedites goose liver lipid accumulation maximization during overfeeding.