Islet β cell mass in diabetes and how it relates to function, birth, and death
Article first published online: 30 JAN 2013
© 2013 New York Academy of Sciences.
Annals of the New York Academy of Sciences
Volume 1281, The Year in Diabetes and Obesity pages 92–105, April 2013
How to Cite
Weir, G. C. and Bonner-Weir, S. (2013), Islet β cell mass in diabetes and how it relates to function, birth, and death. Annals of the New York Academy of Sciences, 1281: 92–105. doi: 10.1111/nyas.12031
- Issue published online: 1 APR 2013
- Article first published online: 30 JAN 2013
- National Institutes of Health. Grant Numbers: [R01 DK 66056, DK 93909
- Joslin Diabetes Research Center. Grant Number: P30 DK36836
- beta cell;
- insulin secretion
In type 1 diabetes (T1D) β cell mass is markedly reduced by autoimmunity. Type 2 diabetes (T2D) results from inadequate β cell mass and function that can no longer compensate for insulin resistance. The reduction of β cell mass in T2D may result from increased cell death and/or inadequate birth through replication and neogenesis. Reduction in mass allows glucose levels to rise, which places β cells in an unfamiliar hyperglycemic environment, leading to marked changes in their phenotype and a dramatic loss of glucose-stimulated insulin secretion (GSIS), which worsens as glucose levels climb. Toxic effects of glucose on β cells (glucotoxicity) appear to be the culprit. This dysfunctional insulin secretion can be reversed when glucose levels are lowered by treatment, a finding with therapeutic significance. Restoration of β cell mass in both types of diabetes could be accomplished by either β cell regeneration or transplantation. Learning more about the relationships between β cell mass, turnover, and function and finding ways to restore β cell mass are among the most urgent priorities for diabetes research.