Taken together these data suggests that if on one hand ethanol may not completely impair the basal expression of many PPARα target genes, on the other hand it severely reduces the ability of the receptor to induce the lipid oxidative metabolism and detoxification systems, as it is required in response to increased fatty acids intake and alcohol consumption. This line of thought seems to be supported by the experiments conducted in PPARα null mice. In fact in these animals several PPARα regulated genes like the peroxisomal acyl-CoA oxidase, the bifunctional enzyme enoyl-CoA:hydratase-3-3-hydroacyl-CoA dehydrogenase, CYP4A and L-FABP were constitutively expressed at levels comparable to wild-type animals [44, 45].
