Clock gene defect disrupts light-dependency of autonomic nerve activity

Hiroki Ikeda, Qing Yong, Takeshi Kurose, Takeshi Todo, Wataru Mizunoya, Tohru Fushiki, Yutaka Seino, Yuichiro Yamada

Research output: Contribution to journalArticlepeer-review

31 Citations (Scopus)


The discovery of clock genes revealed the major molecular components responsible for circadian time-keeping in mammals, but the mechanism by which autonomic nervous system may control circadian rhythm and its relationship to metabolism is unclear. As the Cry1 and Cry2 genes are indispensable for molecular core oscillator function, we investigated autonomic nervous system activity and metabolism in Cry1-/-Cry2-/- mice. The mice were kept in a light-dark cycle, and showed normal circadian locomotor activities including feeding. However, the circadian rhythmicity of oxygen consumption, heart rate, and body temperature were abolished, suggesting hypermetabolism in these mice. Cry1-/-Cry2-/- mice also showed impaired glucose tolerance due to decreased insulin secretion. These results indicate that sympathetic neural activity in Cry1-/-Cry2-/- mice is elevated, reducing adiposity and impairing insulin secretion and suggest that dysregulation of the autonomic nervous system may induce metabolic disorders.

Original languageEnglish
Pages (from-to)457-463
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number3
Publication statusPublished - Dec 21 2007

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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