SREBF1 and Hepatic steatosis: At the molecular level, they activate the peroxisome proliferator-activated receptor alpha (PPARα) and PGC1α (mainly EPA) to enhance FA oxidation, suppress SREBP-1c and ChREBP (primarily DHA), and inhibit DNL and glycolysis, shifting metabolism from lipid synthesis to oxidation, thereby protecting against hepatic steatosis [184].