The Beta Cell in Type 2 Diabetes

被引:111
作者
Christensen, Ashley A. [1 ]
Gannon, Maureen [1 ,2 ,3 ,4 ]
机构
[1] Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Med Ctr, Dept Med, 2213 Garland Ave,MRB 4 7465, Nashville, TN 37232 USA
[3] Tennessee Valley Hlth Author, Dept Vet Affairs, Nashville, TN 37232 USA
[4] Vanderbilt Univ, Dept Cell & Dev Biol, Nashville, TN 37232 USA
关键词
beta-cell dysfunction; Dedifferentiation; Disallowed genes; ER stress; Oxidative stress; beta-cell metabolism; UNFOLDED PROTEIN RESPONSE; ENDOPLASMIC-RETICULUM; ALPHA-CELL; ER STRESS; MITOCHONDRIAL DYNAMICS; TRANSCRIPTION FACTORS; INSULIN-SECRETION; GLUCOSE; EXPRESSION; DEDIFFERENTIATION;
D O I
10.1007/s11892-019-1196-4
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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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页数:8
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