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Division of Endocrinology, The University of Pittsburgh School of Medicine, Pittsburgh PA 15213
* To whom correspondence should be addressed. E-mail: stewart{at}dom.pitt.edu.
In the end, both Types 1 and 2 diabetes result from inadequate production of insulin by the beta cells of the pancreatic islet. Accordingly, strategies that lead to increased pancreatic beta cell mass, as well as retained or enhanced function of islets, would be desirable for the treatment of diabetes. Although pancreatic beta cells have long been viewed as terminally differentiated and irreversibly arrested, evidence now indicates that beta cells can and do replicate, that this replication can be enhanced by a variety of maneuvers, and that beta cell replication plays a quantitatively significant role in maintaining pancreatic beta cell mass and function.
Because beta cells have been viewed as being unable to proliferate, the science of beta 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 beta cell. In this review, we review the molecular details of cell cycle control as they relate to the pancreatic beta 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 beta cell replication, and improving insulin production in animal models as well as in human pancreatic beta cells.
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