• A Khalaileh, T Gonen-Gross, J Magenheim, T Nir, S Porat, S Salpeter, M Stolovich-Rain, A Swisa, N Weinberg, and Y Dor.
• Department of Cellular Biochemistry and Human Genetics, The Institute of Medical Research, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
• Diabetes Obes Metab. 2008 Nov 1; 10 Suppl 4: 128-35.

AbstractRecent 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.

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