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-Cell
Division of Endocrinology, The University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213
* To whom correspondence should be addressed. E-mail: stewart{at}dom.pitt.edu.
Type 1 and type 2 diabetes both result from inadequate production of insulin by the 
-cells of the pancreatic islet. Accordingly, strategies that lead to increased pancreatic -cell mass, as well as retained or enhanced function of islets, would be desirable for the treatment of diabetes. Although pancreatic -cells have long been viewed as terminally differentiated and irreversibly arrested, evidence now indicates that -cells can and do replicate, that this replication can be enhanced by a variety of maneuvers, and that -cell replication plays a quantitatively significant role in maintaining pancreatic -cell mass and function.
Because -cells have been viewed as being unable to proliferate, the science of -cell replication is undeveloped. In the past several years, however, this has begun to change at a rapid pace, and many laboratories are now focused on elucidating the molecular details of the control of cell cycle in the -cell. In this review, we review the molecular details of cell cycle control as they relate to the pancreatic -cell. Our hope is that this review can serve as a common basis and also a roadmap for those interested in developing novel strategies for enhancing -cell replication and improving insulin production in animal models as well as in human pancreatic -cells.
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