Ashley A Christensen1, Maureen Gannon2,3,4,5. 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.
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.
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