The Beta Cell in Type 2 Diabetes
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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.
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.
Keywordsβ-cell dysfunction Dedifferentiation Disallowed genes ER stress Oxidative stress β-cell metabolism
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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