In the liver sections from patients with alcoholic liver diseases, CYP2A expression was detected to be increased (ref. 8). Consistently, in a mouse model, we found that expression of CYP2A and activity of coumarin 7-hydroxylase were induced by alcohol feeding (ref. 9–10). However, alcoholic fatty liver was enhanced in cyp2a5 knockout (cyp2a5−/−) mice, suggesting that CYP2A protects but does not contributes to alcoholic fatty liver (ref. 11–12). In the liver sections from patients with non-alcoholic fatty liver diseases, CYP2A expression was also detected to be increased (ref. 9). In an animal model, hepatic CYP2A protein was reported to be increased in monosodium glutamate-induced obese mice (ref. 13). But it is still unclear whether CYP2A protects against or contributes to obesity and non-alcoholic fatty liver.
