Format

Send to

Choose Destination
Curr Diab Rep. 2019 Aug 9;19(9):81. doi: 10.1007/s11892-019-1196-4.

The Beta Cell in Type 2 Diabetes.

Author information

1
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, 37232, USA.
2
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, 37232, USA. maureen.gannon@vanderbilt.edu.
3
Department of Medicine, Vanderbilt University Medical Center, 2213 Garland Ave, MRB IV 7465, Nashville, TN, 37232, USA. maureen.gannon@vanderbilt.edu.
4
Department of Veterans Affairs, Tennessee Valley Health Authority, Nashville, TN, 37232, USA. maureen.gannon@vanderbilt.edu.
5
Department of Cell & Developmental Biology, Vanderbilt University, Nashville, TN, 37232, USA. maureen.gannon@vanderbilt.edu.

Abstract

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.

KEYWORDS:

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

PMID:
31399863
DOI:
10.1007/s11892-019-1196-4

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center