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The phenomenon of cell regeneration describes the process in which functional cells begin to proliferate to compensate for the loss. Perfect examples are the skin, the liver, the organs that repair themselves after damage.
For three decades, scientists have been examining the potential for regeneration of beta cells, the pancreatic cells responsible for producing insulin.
The beta cell population is partially destroyed when diabetes occurs, and the recovery of these cells presents a unique clinical challenge.
In a new study conducted by the University of Geneva and the University Hospitals of Geneva (HUG), scientists studied diabetic mice to observe the mechanism of regeneration. They observed that this regenerative mechanism was influenced by circadian rhythms – the molecular clocks regulating metabolic functions in a 24-hour cycle of day-night alternation.
Scientists have also identified the important role of the basic clock component BMAL1 in this process.
To explore the link between internal biological clocks and beta cell regeneration, scientists first observed two groups of mice with only 20% beta cells remaining after massive targeted ablation. The mice in the first group were arrhythmic, while the control group had fully functioning clocks.
Volodymyr Petrenko, a researcher in Dr. Dibner’s lab and lead scientist on this study, said: “The result was very clear: the mice with dysfunctional clocks were unable to regenerate their beta cells, and suffered from severe diabetes, while the animals in the control group had their beta cells regenerated; in just a few weeks, their diabetes was under control. By measuring the number of dividing beta cells over 24 hours, the scientists also noted that regeneration is significantly greater at night when mice are active.
“Arrhythmic mice lacked the BMAL1 gene, which encodes the protein of the same name, a transcription factor known for its key activities in the functioning of the circadian clock. Our analyzes show that the BMAL1 gene is essential for the regeneration of beta cells. “
“In addition, large-scale 24-hour transcriptomic analyzes, carried out in collaboration with Prof. Bart Vandereycken at the Department of Mathematics at UNIGE, revealed that the genes responsible for cell cycle regulation and proliferation were not only upregulated, but also acquired circadian rhythmicity.
Dr Charna Dibner, head of the circadian endocrinology laboratory at the Faculty of Medicine of UNIGE, in the departments of medicine, cell physiology and metabolism, said: “BMAL1 indeed seems to be at the heart of our investigation. However, the question of whether regeneration requires functioning circadian clocks themselves, or only BMAL1, whose range of functions goes beyond clocks, remains unclear. That’s what we would like to know for now. “
“Scientists also want to explore the function of alpha cells, which produce glucagon, the hormone that antagonizes insulin, in this model. Arrhythmic mice have indeed shown very high levels of glucagon in the blood. A detailed understanding of these mechanisms must now be pursued, in an attempt to explore the possibility of triggering beta cell regeneration in humans in the future.
To read in the journal Gene and Development, these results allow us to consider new perspectives to promote the regeneration of beta cells.
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