Fig. 6.

Suggested model of fenofibrate-mediated peroxisomal fitness against high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD). HFD or obesity decreases peroxisomal biogenesis and function and increases liver injury, including oxidative stress, inflammation, and fibrosis, due to inhibition of the peroxisome proliferator-activated receptor α (PPARα) pathway. Subsequently, it results in decreased hepatic fatty acid oxidation, increased lipid accumulation, and the induction of liver dysfunction, which leads to the development of NAFLD. Fenofibrate maintains peroxisomal biogenesis and function through activation of the PPARα pathway. It also attenuates liver injury and increases hepatic fatty acid oxidation. Thus, fenofibrate may mediate protective effects against NAFLD by maintaining peroxisomal biogenesis and function.