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Diabetes Obes Metab. 2013 Sep;15 Suppl 3:98-104. doi: 10.1111/dom.12164.

β-Cell differentiation and regeneration in type 1 diabetes.

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  • 1Laboratory of Clinical and Experimental Endocrinology, Campus Gasthuisberg O&N1, Faculty of Medicine, Katholieke Universiteit Leuven, Leuven, Belgium.


Pancreatic insulin-producing β-cells have traditionally been viewed as a quiescent cell population. However, several recent lines of evidence indicated that like most tissues the β-cell mass is dynamically regulated with ongoing β-cell regeneration throughout life to replenish lost or damaged β-cells. In type 1 diabetes (T1D), this fine-tuned balance between β-cell death and β-cell renewal in the endocrine pancreas is lost and the deficit in β-cell mass is largely caused by autoimmune-mediated apoptosis. Currently, the concept that a cure for T1D will require both re-establishment of immunological tolerance along with replacement or regeneration of a functional β-cell mass in T1D patients is generally accepted. In this study our current understanding of the events directing β-cell replication, β-cell reprogramming from different cell types and β-cell regeneration is reviewed, in view of the results of various immunomodulatory strategies aiming at blocking autoimmune responses against pancreatic β-cells and at improving β-cell mass and function in subjects with T1D.

© 2013 John Wiley & Sons Ltd.


regeneration; replication; reprogramming; type 1 diabetes; β-cells

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