Replication confers β cell immaturity

Sapna Puri, Nilotpal Roy, Holger A. Russ, Laura Leonhardt, Esra K. French, Ritu Roy, Henrik Bengtsson, Donald K. Scott, Andrew F. Stewart and Matthias Hebrok ()
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Sapna Puri: University of California
Nilotpal Roy: University of California
Holger A. Russ: University of California
Laura Leonhardt: University of California
Esra K. French: University of Pittsburgh
Ritu Roy: University of California
Henrik Bengtsson: University of California
Donald K. Scott: Icahn School of Medicine at Mount Sinai
Andrew F. Stewart: Icahn School of Medicine at Mount Sinai
Matthias Hebrok: University of California

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract Pancreatic β cells are highly specialized to regulate systemic glucose levels by secreting insulin. In adults, increase in β-cell mass is limited due to brakes on cell replication. In contrast, proliferation is robust in neonatal β cells that are functionally immature as defined by a lower set point for glucose-stimulated insulin secretion. Here we show that β-cell proliferation and immaturity are linked by tuning expression of physiologically relevant, non-oncogenic levels of c-Myc. Adult β cells induced to replicate adopt gene expression and metabolic profiles resembling those of immature neonatal β that proliferate readily. We directly demonstrate that priming insulin-producing cells to enter the cell cycle promotes a functionally immature phenotype. We suggest that there exists a balance between mature functionality and the ability to expand, as the phenotypic state of the β cell reverts to a less functional one in response to proliferative cues.

Date: 2018
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-02939-0

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DOI: 10.1038/s41467-018-02939-0

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