Molecular control of cell cycle progression in the pancreatic beta-cell

Endocr Rev. 2006 Jun;27(4):356-70. doi: 10.1210/er.2006-0004. Epub 2006 Apr 25.


Type 1 and type 2 diabetes both 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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antigens, Viral, Tumor / physiology
  • Cell Cycle / physiology*
  • Cyclin-Dependent Kinases / physiology
  • Cyclins / physiology
  • E2F Transcription Factors / physiology
  • Humans
  • Insulin-Secreting Cells / cytology
  • Insulin-Secreting Cells / physiology*
  • Proto-Oncogene Proteins / physiology
  • Proto-Oncogene Proteins c-mdm2 / physiology
  • Signal Transduction
  • Tumor Suppressor Proteins / physiology


  • Antigens, Viral, Tumor
  • Cyclins
  • E2F Transcription Factors
  • MEN1 protein, human
  • Proto-Oncogene Proteins
  • Tumor Suppressor Proteins
  • Proto-Oncogene Proteins c-mdm2
  • Cyclin-Dependent Kinases