Journal
CURRENT DIABETES REPORTS
Volume 19, Issue 9, Pages -Publisher
CURRENT MEDICINE GROUP
DOI: 10.1007/s11892-019-1196-4
Keywords
beta-cell dysfunction; Dedifferentiation; Disallowed genes; ER stress; Oxidative stress; beta-cell metabolism
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Funding
- Vanderbilt University Training Program in Molecular Endocrinology [5T32 DK7563-30]
- NIH/NIDDK [R01 DK105689, R24DK090964-06]
- VA Merit award [1 I01 BX003744-01]
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Purpose of Review This review summarizes the alterations in the beta-cell observed in type 2 diabetes (T2D), focusing on changes in beta-cell identity and mass and changes associated with metabolism and intracellular signaling. Recent Findings In the setting of T2D, beta-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 beta-cell function and survival. The beta-cell defects leading to T2D likely differ in different individuals and include variations in beta-cell mass, development, beta-cell expansion, responses to ER and oxidative stress, insulin production and secretion, and intracellular signaling pathways. The recent recognition that some beta-cells undergo dedifferentiation without dying in T2D suggests strategies to revive these cells and rejuvenate their functionality.
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