To discuss and study the damage and repair mechanism of the thioacetamide-induced fish liver lesions in our research, firstly we established a liver injury experimental model of grass carp by intraperitoneal injection of thioacetamide (TAA). Then fish were fed with additive yeast culture dv, curcumin and silymarin for 70 days, and the hepatopancreas samples were collected. We used real-time quantitative reverse transcription polymerase chain reaction (qPCR) method to detect the mRNA abundance of FAS, PGC1-α, SCD1, UCP2, PPAR-α, PPAR-γ and IGF-Ⅰso as to discuss the changes of the expression activity of the lipid metabolism-related genes of hepatopancreas of fishes in the experimental models as well as that which were fed with the three damage-repair additives such as yeast culture dv, curcumin and silymarin. The results showed that, after the thioacetamide induced liver injury, the expression level of FAS was significantly increased, the upstream genes regulating the lipid catabolism such as PPAR-α, ΡΡΑR-γ and PGC1-α had no significant change, while the SCD1 was significantly reduced, which may result in the increased lipid accumulation in the liver cells, so as to induce the occurrence and development of fatty liver disease. In brief, after feeding additives such as yeast culture dv, curcumin and silymarin, thioacetamide induced damage of the lipid metabolism of the grass carp hepatopancreas was to some extent repaired.