Biomedicine

A Case of Lost Identity?

See allHide authors and affiliations

Science  05 Oct 2012:
Vol. 338, Issue 6103, pp. 17
DOI: 10.1126/science.338.6103.17-d
CREDIT: C. TALCHAI ET AL., CELL 150 (14 SEPTEMBER 2012) ©2012 ELSEVIER INC.

As the cells responsible for the secretion of insulin—the major hormonal regulator of blood glucose levels—pancreatic β cells are the central command center for the prevention of type 2 diabetes. When β cells cannot keep pace with metabolic demands (which occurs with obesity, during pregnancy, and as people age), insulin secretion drops and blood glucose levels rise. The prevailing model is that β cells fail because they are lost through programmed cell death and are not replaced. Studying several mouse models of diabetes, Talchai et al. present evidence for a radically different mechanism of β cell failure: They propose that the loss of β cells occurs because under conditions of physiological stress, the cells change their identity through de-differentiation to a more progenitor-like state and are then converted to other pancreatic cell types that do not secrete insulin, such as α cells. The transcription factor FoxO1 plays an essential role in keeping β cells in their differentiated state. If these observations apply to humans, they would suggest that therapies for type 2 diabetes should focus on reversing the β cell de-differentiation process rather than promoting β cell replication.

Cell 150, 1223 (2012).

Navigate This Article