Pancreatic Ppy-expressing γ-cells display mixed phenotypic traits and the adaptive plasticity to engage insulin production

Marta Perez-Frances, Léon van Gurp, Maria Valentina Abate, Valentina Cigliola, Kenichiro Furuyama, Eva Bru-Tari, Daniel Oropeza, Taïna Carreaux, Yoshio Fujitani, Fabrizio Thorel and Pedro L. Herrera ()
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Marta Perez-Frances: University of Geneva
Léon van Gurp: University of Geneva
Maria Valentina Abate: University of Geneva
Valentina Cigliola: University of Geneva
Kenichiro Furuyama: University of Geneva
Eva Bru-Tari: University of Geneva
Daniel Oropeza: University of Geneva
Taïna Carreaux: University of Geneva
Yoshio Fujitani: Gunma University
Fabrizio Thorel: University of Geneva
Pedro L. Herrera: University of Geneva

Nature Communications, 2021, vol. 12, issue 1, 1-16

Abstract: Abstract The cellular identity of pancreatic polypeptide (Ppy)-expressing γ-cells, one of the rarest pancreatic islet cell-type, remains elusive. Within islets, glucagon and somatostatin, released respectively from α- and δ-cells, modulate the secretion of insulin by β-cells. Dysregulation of insulin production raises blood glucose levels, leading to diabetes onset. Here, we present the genetic signature of human and mouse γ-cells. Using different approaches, we identified a set of genes and pathways defining their functional identity. We found that the γ-cell population is heterogeneous, with subsets of cells producing another hormone in addition to Ppy. These bihormonal cells share identity markers typical of the other islet cell-types. In mice, Ppy gene inactivation or conditional γ-cell ablation did not alter glycemia nor body weight. Interestingly, upon β-cell injury induction, γ-cells exhibited gene expression changes and some of them engaged insulin production, like α- and δ-cells. In conclusion, we provide a comprehensive characterization of γ-cells and highlight their plasticity and therapeutic potential.

Date: 2021
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DOI: 10.1038/s41467-021-24788-0

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