The decrease in PPAR-α produced by ethanol in WT and KI mice may contribute to the development of fatty liver by decreasing fatty acid oxidation. This remains to be evaluated. With respect to fatty acid synthesis, we could not detect increases in SREBP, acetyl CoA carboxylase or fatty acyl synthase levels in the ethanol-fed WT or KI mice. However, as found by other [54,55] levels of stearoyl CoA desaturase-1 were increased by ethanol in the WT mice as well as the KO and the KI mice. SCD-1 has been shown to promote hepatic steatosis as SCD-1 deficiency prevents liver steatosis in various mouse models [56,57]. Oleate, the product of the SCD-1 catalyzed desaturation of stearic acid normalized the decreased hepatic lipogenesis of the SCD -1 KO mice, and it has been suggested that endogenous oleate synthesis catalyzed by SCD-1 acts as a metabolic switch which influences the balance of energy (fat) storage versus energy (fat) oxidation [57]. SCD-1 deficiency increases the phosphorylation state of AMPK and hepatic AMPK activity [58], hence, elevating SCD-1 would inactivate AMPK, thereby promoting lipogenesis. However,
