Weir, GordonBonner-Weir, Susan2014-02-182013Weir, Gordon C., and Susan Bonner-Weir. 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 (1): 92-105. doi:10.1111/nyas.12031. http://dx.doi.org/10.1111/nyas.12031.0077-8923http://nrs.harvard.edu/urn-3:HUL.InstRepos:11717631In 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.en-USbeta cellisletsdiabetesneogenesisinsulin secretionJournal Article2014-02-1810.1111/nyas.12031