Deranged lipid metabolism and steatosis is one of the hallmark of heavy ethanol consumption. The role of nuclear receptors (especially PPARα) in the control of lipid metabolism is well known and has been already extensively reviewed [1, 2, 116, 117]; however, some specific effects, observed in ethanol fed-animals and previously ascribed to the PPARα pathway, could indeed be RXR specific [98, 118]. When fastened or treated with WY14,643, RXR null mice show a phenotype in several aspects different from PPAR null mice. Apolipoprotein A-I and C-III mRNA levels, serum cholesterol and triglyceride levels are markedly induced in untreated RXR null but not in PPARα-null mice. Moreover, fasting-induced PPARα activation and WY14,643 effects are reduced in RXR KO mice. Acyl-CoA oxidase, medium chain acyl-CoA dehydrogenase, and malic enzyme induction by WY14,643 are reduced in null mice without altering their mRNA levels [118].
