droplets (8). These results suggest that human CYP2A6 may participate in the regulation of lipid metabolism for the development of both alcoholic and non-alcoholic fatty liver. Kirby et al first proposed the notion that CYP2A5 may involve hepatic lipid metabolism (3). Here we found that the ethanol-induced liver content of TG, as well as the serum levels of TG and glucose, were higher in cyp2a5−/− mice than cyp2a5+/+ mice; similarly, alcoholic fatty liver was also more pronounced in cyp2a5−/− than cyp2a5+/+ mice. In another model, after high-fat diet feeding, the body weight was increased more rapidly in cyp2a5−/− than cyp2a5+/+ mice and fatty liver was more pronounced in cyp2a5−/− than cyp2a5+/+ mice (unpublished results). The results for both alcoholic and non-alcoholic fatty liver animal models suggest that CYP2A5 contributes to hepatic lipid metabolism. FAS and AOX are two major enzymes involved in lipid metabolism. In the present study, we found that the basal levels of FAS and AOX are higher in cyp2a5−/− than cyp2a5+/+ mice, suggesting that there is a more active lipid metabolism in cyp2a5−/− mice than cyp2a5+/+ mice. After ethanol feeding, FAS was comparably decreased in cyp2a5−/− and cyp2a5+/+ mice, while AOX was decreased in cyp2a5−/− mice but
