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Diabetes Obes Metab. 2008 Nov;10 Suppl 4:128-35. doi: 10.1111/j.1463-1326.2008.00948.x.

Determinants of pancreatic beta-cell regeneration.

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1
Department of Cellular Biochemistry and Human Genetics, The Institute of Medical Research, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.

Abstract

Recent studies have revealed a surprising plasticity of pancreatic beta-cell mass. beta-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 beta-cells, by beta-cell regeneration. The major cellular source for new beta-cells following specific ablation, as well as during normal homeostatic maintenance of adult beta-cells, is proliferation of differentiated beta-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 beta-cells. The molecular triggers for enhanced beta-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.

[Indexed for MEDLINE]

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