BackgroundUnlike mammals, goose fatty liver shows a strong tolerance to fatty acids without obvious injury. Stearyl-coenzyme A desaturase 1 (SCD1) serves crucial role in desaturation of saturated fatty acids (SAFs), but its role in the SAFs tolerance of goose hepatocytes has not been reported. This study was conducted to explore the role of SCD1 in regulating palmitic acid tolerance of goose primary hepatocytes.MethodsTo evaluate the palmitic acid tolerance of cultured hepatocytes, MTT was examined to reflect the effect of palmitic acid on cell viability, and quantitative PCR was used to detect the mRNA expression levels of several genes related to ER stress, inflammation, and apoptosis, and the role of SCD1 in palmitic acid tolerance of goose hepatocytes was explored using RNA interfere.ResultsOur results indicated that goose hepatocytes exhibited a higher tolerant capacity to palmitic acid than human hepatic cell line (LO2 cells). Furthermore, the mRNA levels of fatty acid desaturation-related genes (SCD1 and FADS2) and fatty acid elongate enzyme-related gene (ELOVL6) were significantly upregulated in goose primary hepatocytes treated with 0.6 mM palmitic acid. However, in cultured LO2 cells, expression of ER stress-related genes (XBP, BIP and ATF6), inflammatory response-related genes (IL-6, IL-1β and IFN-γ) and apoptosis-related genes (Bax, Bcl-2, Caspase-3 and Caspase-9) was significantly enhanced by the addition of 0.6 mM palmitic acid. Additionally, siRNA-mediated downregulation of SCD1 significantly reduced the palmitic acid tolerance of goose primary hepatocytes under the treatment of 0.6 mM palmitic acid; meanwhile, the mRNA expression of inflammatory-related genes (IL-6 and IL-1β) and several key genes involved in the PI3K/AKT, FoxO1, mTOR and AMPK pathways (AKT1, AKT2, FOXO1 and SIRT1), as well as the protein expression of cytochrome C and the apoptosis rate were also upregulated.ConclusionIn conclusion, our data suggested that SCD1 is involved in enhancing the palmitic acid tolerance of goose primary hepatocytes by regulating inflammation- and apoptosis-related genes expression.