I had recently the great pleasure to contribute to a collaboration study led by Dr. Charna Dibner (from the Division of Endocrinology, Diabetes, Hypertension and Nutrition, Department of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva) deciphering the regenerative mechanisms acting in endocrine pancreatic cells. The results of this study were published today, and we show that:
- The main goal of this study was to explore the connection between internal biological clocks and beta cell regeneration.
- Pancreatic islets with only 20% beta cells remaining after targeted ablation by doxycycline-induced expression of diphtheria toxin A (DTA) in Insulin-rtTA/TET-DTA mice, which resulted in an acute hyperglycemia, showed dramatic changes in gene expression in residual β cells, and only temporal alterations of gene expression in α cells.
- The mice bearing dysfunctional clocks were unable to regenerate their beta cells, and suffered from severe diabetes, while the control group animals had their beta cells regenerated.
- No compensatory β-cell proliferation was observed in arrhythmicBmal1-deficient mice, which lack circadian clocks.
Continue your reading here:
Authors: Volodymyr Petrenko, Miri Stolovich-Rain, Bart Vandereycken, Laurianne Giovannoni, Kai-Florian Storch, Yuval Dor, Simona Chera and Charna Dibner
Genes and Development 2020 13 November 2020
DOI information: http://www.genesdev.org/cgi/doi/10.1101/gad.343137.120