Preclinical18–21 and clinical22 studies highlight that PPARα influences NAFLD and NASH. Mice lacking PPARα develop steatosis during fasting,7 8 suggesting the importance of PPARα activity for using FFA released from adipocytes. However, PPARα is expressed and active in many tissues, including skeletal muscles,23 adipose tissues,24 25 intestines,26 kidneys27 and heart,28 which all contribute to fatty acid homeostasis. Therefore, it remains unknown whether the increased steatosis susceptibility in mice lacking PPARα depends on PPARα activity only in hepatocytes or also in other organs.
