encoding acyl-CoA oxidase, carnitine palmitoyltransferase I and short chain acyl-CoA dehydrogenase (Kersten et al., 1999; Leone et al., 1999). After fasting, Pparα−/− mice develop more severe fatty liver due to impaired fat oxidation, but expression of carnitine palmitoyltransferase I and short chain acyl-CoA dehydrogenase is similar in fasted Pparα−/− and wild-type mice (Kersten et al., 1999). Alcoholic fatty liver disease was more pronounced in Pparα−/− mice, however, acyl-CoA oxidase levels were still comparable in Pparα−/− mice and wild-type mice (Okiyama et al., 2009). These results suggest that other PPARα-dependent mechanisms may occur and blunt fatty liver.
