Determinants of pancreatic β-cell regeneration

A. Khalaileh, T. Gonen-gross, J. Magenheim, T. Nir, S. Porat, S. Salpeter, M. Stolovich-rain, A. Swisa, N. Weinberg, Yuval Dor*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Recent studies have revealed a surprising plasticity of pancreatic β-cell mass. β-cell mass is now recognized to increase and decrease in response to physiological demand, for example during pregnancy and in insulin-resistant states. Moreover, we and others have shown that mice recover spontaneously from diabetes induced by killing of 70-80% of β-cells, by β-cell regeneration. The major cellular source for new β-cells following specific ablation, as well as during normal homeostatic maintenance of adult β-cells, is proliferation of differentiated β-cells. More recently, it was shown that one form of severe pancreatic injury, ligation of the main pancreatic duct, activates a population of embryonic-type endocrine progenitor cells, which can differentiate into new β-cells. The molecular triggers for enhanced β-cell proliferation during recovery from diabetes and for activation of embryonic-type endocrine progenitors remain unknown and represent key challenges for future research. Taken together, recent data suggest that regenerative therapy for diabetes may be a realistic goal.

Original languageAmerican English
Pages (from-to)128-135
Number of pages8
JournalDiabetes, Obesity and Metabolism
Issue numberSUPPL. 4
StatePublished - 2008


  • Islets
  • Lineage tracing
  • Proliferation
  • Regeneration
  • Transgenic mice
  • β-cells


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