Our results can be attributed to the capacity of n-3 PUFA acting in the positive regulation of PPAR expression, which codifies proteins involved in FA oxidation, and in the negative regulation of SREBP-1 and SREBP-2, codifying the proteins of lipidic synthesis, decreasing the availability of free FAs and hepatic steatosis [56]. This evidence concerns the gene SREBF2 and Hepatic steatosis.