SREBF1 and steatosis: Oxidative stress and related reactive intermediates may contribute, as proposed for ethanol, to the genesis of steatosis by negatively affecting secretion of lipoproteins (either by enhancing degradation of Apo-B100 or by affecting lipoprotein glycosylation in the Golgi apparatus) [135,140] or even by interfering with the regulation of lipid synthesis by the sterol regulatory element binding protein 1 (SREBP-1) or the peroxisome proliferator-activated receptor α (PPAR- α) [156].