It is found that anethol trithione (H2S donor) can significantly reduce ACC1 and FAS expression and SCD1 expression, up-regulate FADS1 and FADS2 and inhibit 
de novo synthesis of toxic saturated fattyacid (
palmitic acid), inhibit the synthesis of 
oleic acid, promote the desaturation of 
fatty acid and adjust the proportion of n-3 / n-6 
polyunsaturated fatty acid under the condition of high-
fat diet.Meanwhile, PAQR3 is inhibited to promote 
peroxidase body oxidation of lipid and degradation of LDL; in addition, the expression quantity of RTN3 can be reduced, so that the overexpression of SREPB1c is reduced, and the formation of liver 
cell fat droplets is reduced; the reduced expression of FATP2, FATP4, FATP5 and L-FABP can be up-regulated, which indicates that the 
drug enhances 
fatty acid uptake of hepatocytes and promotes transport of the hepatocytes; it is particularly noticed that anethol trithione can remarkably increase the expression quantity of Mitofusin 1, Mitofusin 2 and CPT1a, mitochondrial fusion is promoted, beta-oxidation of 
fatty acid is enhanced, and the anethol trithione is widely applied to damage of toxic fatty acid to organs such as heart, brain, 
liver and kidney.