the molecular mechanism of ER stress response in pancreatic beta cells : type 2 diabets

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In the current study, we investigated 4E-BP1 expression, which is important for beta-cell survival, in MIN6 cells under ER stress and oxidative stress. We found that JNK activated by oxidative stress is involved in the modulation of 4E-BP1 expression and phosphorylation in MIN6 cells.In this study, we analyzed Atf6α-null mice. ATF6α protects β-cells from ER stress and suppresses hepatosteatosis, but plays a role in the development of hyperlipidemia and insulin resistance.The study is designed to investigate whether the activation of the incretin system by DPP-4 inhibition ameliorates β-cell failure in WFS1-deficient mice, a genetically defined model of human diabetes caused by ER stress in β-cells. These findings provide evidence that activation of the incretin system by vildagliptin plays a protective role against β-cells with WFS1-deficiency.