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Disruption of the clock components CLOCK and BMAL1 leads to hypoinsulinaemia and diabetes
Disrupting key body clock proteins CLOCK and BMAL1 may cause low insulin levels and diabetes
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Abstract
Pancreatic islets exhibit circadian gene and protein oscillations of key transcription factors that may influence insulin secretion.
- The transcription factors CLOCK and BMAL1 display self-sustained circadian oscillations in pancreatic islets.
- In circadian mutant mice, the timing of oscillation for genes related to growth, glucose metabolism, and insulin signaling is delayed.
- Mutant mice lacking Clock and Bmal1 show impaired glucose tolerance and reduced insulin secretion, with worsening defects in islet size and proliferation as they age.
- Disruption of the Clock gene leads to widespread changes in the expression of islet genes linked to growth, survival, and vesicle assembly.
- Conditional removal of the pancreatic circadian clock can result in diabetes mellitus due to impaired beta-cell function.
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