Characteristic Gene Alterations During Fatty Acid Metabolism in the Goose Liver

The development of hepatic steatosis in geese is a complex, multistage process involving genes related to lipid synthesis, transport, storage, and metabolism. Key genes activated during this process include ME1 (malic enzyme 1), SCD1 (stearoyl-CoA desaturase), ACSL1 (acyl-CoA synthetase long-chain family member 1), and ELOVL6 (elongation of very-long-chain fatty acids protein 6). The expression of these genes varies depending on the tissue, breed, and metabolic context. Geese possess a unique ability to develop hepatic steatosis (fatty liver) without accompanying inflammation or liver damage. This condition typically arises from overfeeding, either through carbohydrates or fats, leading to significant triglyceride accumulation in hepatocytes. Importantly, this state remains reversible and is considered non-pathological. The physiological and molecular changes observed in overfed geese, particularly regarding liver lipid accumulation and serum enzyme activity, closely resemble those found in human non-alcoholic fatty liver disease (NAFLD). This similarity makes geese an excellent biomedical model for studying NAFLD. Overfeeding initiates a cascade of enzymatic reactions that regulate lipid metabolism at the genetic level. These reactions decrease circulating free fatty acids and glucose while promoting triglyceride storage in the liver. The aim of this study is to synthesize current knowledge on the genetic regulation of fatty acid metabolism in geese, highlighting how these genes coordinate the processes of activation, desaturation, synthesis, and elongation during induced steatosis. Moreover, the summarized effects of different diet supplements will enhance goose feeding strategies for foie gras production.