Fabrizio Thorel

TL;DR: In this article, a transgenic model of diphtheria-toxin-induced acute selective near-total beta-cell ablation was used to investigate whether adult mammals can differentiate (regenerate) new beta-cells after extreme, total β-cell loss, as in diabetes.

TL;DR: It is found that senescence does not alter α-cell plasticity: α-cells can reprogram to produce insulin from puberty through to adulthood, and also in aged individuals, even a long time after β-cell loss.

TL;DR: These findings establish Nkx6.1 as a beta cell programming factor and demonstrate that repression of alternative lineage programs is a fundamental principle by which beta cells are specified and maintained.

TL;DR: B-cell regeneration in a transgenic model of diphtheria-toxin-induced acute selective near-total b-cell ablation is shown and could be harnessed towards methods of producing b-cells for diabetes therapies, either in differentiation settings in vitro or in induced regeneration.

TL;DR: It is revealed that Pdx1 can work single-handedly as a potent context-dependent autonomous reprogramming agent, and a postnatal differentiation evaluation stage involved in normal endocrine maturation is suggested.