Role of PPARα in control of torpor through FGF21-NPY pathway: From circadian clock genes to seasonal change and cardiovascular disease

Abstract

In nature, hibernating animals experience fasting, cold temperature, and short day seasonally. Torpor is a state of decreased physiological activity in an animal, usually characterized by a reduced body temperature and rate of metabolism to adapt to such a severe environment. Ablation of the central clock synchronizer, the suprachiasmatic nucleus in brain, abolishes torpor, a hibernation-like state, implicating the circadian clock involved in this seasonal change. Biologists know well that the energy source of daily heterotherms/hibernators change from glucose to lipids in winter. Here we review several lines of evidence of a master transcriptional regulator in lipid catabolism, peroxisome proliferator-activated receptor α (PPARα), in the control of torpor through the fibroblast growth factor 21—neuropeptide Y (FGF21—NPY) pathway.1 Furthermore, we showed the role of PERIOD2 protein as a suppressor of plasminogen activator inhibitor-1(PAI-1) gene expression using PER2 transgenic mice. These indicates the importance of clock genes to tell seasons to improve and cardiovascular function.