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Abstract
In vivo regeneration of β cells provides hope for self-renewal of functional insulin-secreting cells following β-cell failure, a historically fatal condition now sustainable only by administration of exogenous insulin. Despite advances in the treatment of diabetes mellitus, the path toward endogenous renewal of β-cell populations has remained elusive. Intensive efforts have focused on elucidating pancreatic transcriptional programs that can drive the division and (trans-)differentiation of non-β cells to produce insulin. A surprise has been the identification of an essential role of the molecular circadian clock in the regulation of competent insulin-producing β cells. In this issue of Genes & Development, work by Petrenko and colleagues (pp. 1650-1665) now shows a requirement for the intrinsic clock in the regenerative capacity of insulin-producing cells following genetic ablation of β cells. These studies raise the possibility that enhancing core clock activity may provide an adjuvant in cell replacement therapies.
Highlights
To obesity and hypoinsulinemic diabetes—a hallmark of β-cell failure in human diabetes (Perelis et al 2015)
New insulin-secreting cells were observed within islets once devoid of β cells, and genetic tracing of pancreatic cell types revealed that a substantial proportion of these insulin-secreting cells arose from either non-β cells or β-cell precursors
In which doxycycline-induced expression of diphtheria toxin A (DTA) triggers β-cell destruction, Petrenko et al (2020) inquired whether the circadian clock might be required for the regeneration of functional insulin-secreting cells by comparing responses to doxycycline following knockout of the gene encoding the core clock activator BMAL1
Summary
To obesity and hypoinsulinemic diabetes—a hallmark of β-cell failure in human diabetes (Perelis et al 2015). Thorel et al (2010) established a powerful genetic model to examine β-cell regeneration by showing that seemingly terminally differentiated adult pancreatic cells could be converted to insulin-secreting cells in vivo following diphtheria-induced β-cell ablation during adulthood. In which doxycycline-induced expression of diphtheria toxin A (DTA) triggers β-cell destruction, Petrenko et al (2020) inquired whether the circadian clock might be required for the regeneration of functional insulin-secreting cells by comparing responses to doxycycline following knockout of the gene encoding the core clock activator BMAL1.
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