However, the induction of both peroxisomal and mitochondrial β-oxidation pathways by clofibrate or WY14,643 was completely abolished in PPARα−/− mice [41, 45, 46]. Moreover, PPARα null mice were found to have a marked reduction in the expression of ALDH, which led to increased acetaldehyde levels, increased lipid peroxidation and oxidative stress. PPARα null mice were thus significantly more sensitive to ethanol induced liver damage than wild-type animals [41].
