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

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.

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Cited by papers we hold 4

• Extracellular Vesicles Derived Human-miRNAs Modulate the Immune System in Type 1 Diabetes · 2020
  Not checked
• Diabetes causes marked inhibition of mitochondrial metabolism in pancreatic β-cells · 2019
  No notice
• Roles of lncRNAs in Pancreatic Beta Cell Identity and Diabetes Susceptibility · 2014
  Not checked
• Reversible changes in pancreatic islet structure and function produced by elevated blood glucose · 2014
  No notice

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