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Obesity and metabolic syndrome in circadian Clock mutant mice. 2005
Fred W Turek, and
Corinne Joshu, and
Akira Kohsaka, and
Emily Lin, and
Ganka Ivanova, and
Erin McDearmon, and
Aaron Laposky, and
Sue Losee-Olson, and
Amy Easton, and
Dalan R Jensen, and
Robert H Eckel, and
Joseph S Takahashi, and
Joseph Bass
Department of Neurology, Northwestern University, Evanston, IL 60208, USA.
The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus. We found that homozygous Clock mutant mice have a greatly attenuated diurnal feeding rhythm, are hyperphagic and obese, and develop a metabolic syndrome of hyperleptinemia, hyperlipidemia, hepatic steatosis, hyperglycemia, and hypoinsulinemia. Expression of transcripts encoding selected hypothalamic peptides associated with energy balance was attenuated in the Clock mutant mice. These results suggest that the circadian clock gene network plays an important role in mammalian energy balance.
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