A healthy liver does not accumulate lipids, but it plays central roles in fatty acid anabolism and export to peripheral organs, including white adipose tissue for energy storage.4 During dietary restriction, hepatic fatty acid catabolism is also critical for using free fatty acids (FFAs) released from white adipose tissues. PPARα is the most abundant isotype in hepatocytes and is involved in many aspects of lipid metabolism,5 6 including fatty acid degradation, synthesis, transport, storage, lipoprotein metabolism and ketogenesis during fasting.7–9 In addition, PPARα controls glycerol use for gluconeogenesis9 as well as autophagy10 in response to fasting. Moreover, PPARα regulates the expression of the fibroblast growth factor 21 (FGF21) during starvation.11 12 In turn, FGF21 acts as an endocrine hormone targeting various functions including metabolic control.13 Finally, PPARα helps repress the acute-phase response and inflammation in the liver.14
