Current Diabetes Reports

, 19:81 | Cite as

The Beta Cell in Type 2 Diabetes

  • Ashley A. Christensen
  • Maureen GannonEmail author
Pathogenesis of Type 2 Diabetes and Insulin Resistance (M-E Patti, Section Editor)
Part of the following topical collections:
  1. Topical Collection on Pathogenesis of Type 2 Diabetes and Insulin Resistance


Purpose of Review

This review summarizes the alterations in the β-cell observed in type 2 diabetes (T2D), focusing on changes in β-cell identity and mass and changes associated with metabolism and intracellular signaling.

Recent Findings

In the setting of T2D, β-cells undergo changes in gene expression, reverting to a more immature state and in some cases transdifferentiating into other islet cell types. Alleviation of metabolic stress, ER stress, and maladaptive prostaglandin signaling could improve β-cell function and survival.


The β-cell defects leading to T2D likely differ in different individuals and include variations in β-cell mass, development, β-cell expansion, responses to ER and oxidative stress, insulin production and secretion, and intracellular signaling pathways. The recent recognition that some β-cells undergo dedifferentiation without dying in T2D suggests strategies to revive these cells and rejuvenate their functionality.


β-cell dysfunction Dedifferentiation Disallowed genes ER stress Oxidative stress β-cell metabolism 


Funding Information

Ashley A. Christensen was supported in part by the Vanderbilt University Training Program in Molecular Endocrinology (5T32 DK7563-30). Maureen Gannon was supported by grants from the NIH/NIDDK (R01 DK105689 and R24DK090964-06) and by a VA Merit award (1 I01 BX003744-01).

Compliance with Ethical Standards

Conflict of Interest

The authors declare that they have no conflict of interest.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.


Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance

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Authors and Affiliations

  1. 1.Department of Molecular Physiology and Biophysics, Vanderbilt UniversityNashvilleUSA
  2. 2.Department of MedicineVanderbilt University Medical CenterNashvilleUSA
  3. 3.Department of Veterans Affairs, Tennessee Valley Health AuthorityNashvilleUSA
  4. 4.Department of Cell & Developmental BiologyVanderbilt UniversityNashvilleUSA

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