Disruption of the clock components CLOCK and BMAL1 leads to hypoinsulinaemia and diabetes

Biliana Marcheva, Kathryn Moynihan Ramsey, Ethan D. Buhr, Yumiko Kobayashi, Hong Su, Caroline H. Ko, Ganka Ivanova, Chiaki Omura, Shelley Mo, Martha H. Vitaterna, James P. Lopez, Louis H. Philipson, Christopher A. Bradfield, Seth D. Crosby, Lellean JeBailey, Xiaozhong Wang, Joseph S. Takahashi and Joseph Bass ()
Additional contact information
Biliana Marcheva: Northwestern University Feinberg School of Medicine
Kathryn Moynihan Ramsey: Northwestern University Feinberg School of Medicine
Ethan D. Buhr: Northwestern University
Yumiko Kobayashi: Northwestern University Feinberg School of Medicine
Hong Su: Molecular Biology and Cell Biology, Northwestern University
Caroline H. Ko: Northwestern University
Ganka Ivanova: Northwestern University Feinberg School of Medicine
Chiaki Omura: Northwestern University Feinberg School of Medicine
Shelley Mo: Weinberg College of Arts and Sciences, Northwestern University
Martha H. Vitaterna: Center for Sleep and Circadian Biology, Northwestern University
James P. Lopez: University of Chicago
Louis H. Philipson: University of Chicago
Christopher A. Bradfield: McArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health
Seth D. Crosby: Washington University School of Medicine
Lellean JeBailey: GeneGo Inc.
Xiaozhong Wang: Molecular Biology and Cell Biology, Northwestern University
Joseph S. Takahashi: University of Texas Southwestern Medical Center
Joseph Bass: Northwestern University Feinberg School of Medicine

Nature, 2010, vol. 466, issue 7306, 627-631

Abstract: Clocking on to diabetes During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis — a rhythmic process that is disturbed in people with diabetes. Experiments in mice now show that the pancreatic islets contain their own biological clock, which orchestrates insulin secretion during the sleep–wake cycle. The transcription factors CLOCK and BMAL1 are vital for this process, and mice with defective copies of the genes Clock and Bmal1 develop hypoinsulinaemia and diabetes. By demonstrating that a local tissue clock integrates circadian and metabolic signals in pancreatic β-cells, this work suggests that circadian analyses are crucial for deeper understanding of metabolic phenotypes, as well as for the treatment of metabolic diseases such as type 2 diabetes.

Date: 2010
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DOI: 10.1038/nature09253

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