Systemic regulation of the age-Related decline of pancreatic β-Cell replication

Seth J. Salpeter, Abed Khalaileh, Noa Weinberg-Corem, Oren Ziv, Benjamin Glaser, Yuval Dor*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

100 Scopus citations

Abstract

The frequency of pancreatic β-cells replication declines dramatically with age, potentially contributing to the increased risk of type 2 diabetes in old age. Previous studies have shown the involvement of cell-Autonomous factors in this phenomenon, particularly the decline of polycomb genes and accumulation of p16/INK4A. Here, we demonstrate that a systemic factor found in the circulation of young mice is able to increase the proliferation rate of old pancreatic β-cells. Old mice parabiosed to young mice have increased β-cells replication compared with unjoined old mice or old mice parabiosed to old mice. In addition, we demonstrate that old β-cells transplanted into young recipients have increased replication rate compared with cells transplanted into old recipients; conversely, young β-cells transplanted into old mice decrease their replication rate compared with young cells transplanted into young recipients. The expression of p16/INK4A mRNA did not change in heterochronic parabiosis, suggesting the involvement of other pathways. We conclude that systemic factors contribute to the replicative decline of old pancreatic β-cells.

Original languageAmerican English
Pages (from-to)2843-2848
Number of pages6
JournalDiabetes
Volume62
Issue number8
DOIs
StatePublished - Aug 2013

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