Global prevalence of non-alcoholic fatty liver disease (NAFLD) constitutes a threat to human health. Goose is a unique model of NAFLD for discovering therapeutic targets as its liver can develop severe steatosis without overt injury. Fatty acid desaturase (Fads) is a potential therapeutic target as Fads expression and mutations are associated with liver fat. Here， we hypothesized that Fads was promoted to provide a protection for goose fatty liver. To test this， goose Fads1 and Fads2 were sequenced. Fads1/2/6 expression was determined in goose liver and primary hepatocytes by quantitative PCR. Liver fatty acid composition was also analyzed by gas chromatography. Data indicated that hepatic Fads1/2/6 expression was gradually increased with the time of overfeeding. In contrast， trans-C18:1n9 fatty acid (Fads inhibitor) was reduced. However， enhanced Fads capacity for long-chain polyunsaturated fatty acid (LC-PUFA) synthesis was not sufficient to compensate for the depleted LC-PUFAs in goose fatty liver. Moreover， cell studies showed that Fads1/2/6 expression was regulated by fatty liver-associated factors. Together， these findings suggest Fads1/2 as protective components are promoted to meet instant need for LC-PUFAs in goose fatty liver， and we propose this is required for severe hepatic steatosis without liver injury.