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Ann N Y Acad Sci. 2013 Apr;1281:92-105. doi: 10.1111/nyas.12031. Epub 2013 Jan 30.

Islet β cell mass in diabetes and how it relates to function, birth, and death.

Author information

1
Section on Islet Cell Biology and Regenerative Medicine, Research Division, Joslin Diabetes Center, Department of Medicine, Harvard Medical School, Boston, MA 02215, USA. gordon.weir@joslin.harvard.edu

Abstract

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.

PMID:
23363033
PMCID:
PMC3618572
DOI:
10.1111/nyas.12031
[Indexed for MEDLINE]
Free PMC Article

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