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PPAR Research
Volume 2009, Article ID 412949, 5 pages
Review Article

Role of PPAR in the Control of Torpor through FGF21-NPY Pathway: From Circadian Clock to Seasonal Change in Mammals

1Clock Cell Biology, Department of Biological Resources and Functions, National Institute of Advanced Industrial Science and Technology (AIST), 6-5 Tsukuba Center, 1-1 Higashi, Tsukuba, 305-8566, Japan
2Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8502, Japan

Received 18 December 2008; Revised 3 March 2009; Accepted 2 April 2009

Academic Editor: Richard P. Phipps

Copyright © 2009 Norio Ishida. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


In nature, hibernating animals encounter 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 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 knows well the energy source of daily heterotherms/hibernators changed from glucose to lipids in winter. Here we review several lines of evidence of a master transcriptional regulator in lipid catabolism, PPAR , in the control of torpor through FGF21-NPY pathway. This indicate the importance of circadian—and photoperiod—regulation of PPAR to tell seasons in our body.