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Ting Xiao, Xiuci Liang, Hailan Liu, Feng Zhang, Wen Meng, and Fang Hu

Introduction Endoplasmic reticulum (ER) stress due to high fat diet (HFD) feeding or genetic obesity is associated with hepatic steatosis and insulin resistance ( Kammoun et al . 2009 , Yoshiuchi et al . 2009 , Ye et al . 2010 , Meng et

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Liping Luo, Wanxiang Jiang, Hui Liu, Jicheng Bu, Ping Tang, Chongyangzi Du, Zhipeng Xu, Hairong Luo, Bilian Liu, Bo Xiao, Zhiguang Zhou, and Feng Liu

ER stress, leading to UPR and impaired lipid homeostasis ( Ron & Walter 2007 , Rutkowski et al . 2008 , Walter & Ron 2011 ). While long-term HFD feeding and genetic obesity have been well-documented to induce chronic ER stress associated with

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Fabio Arturo Grieco, Andrea Alex Schiavo, Flora Brozzi, Jonas Juan-Mateu, Marco Bugliani, Piero Marchetti, and Décio L Eizirik

systems taking place during insulitis ( Eizirik et al. 2009 , 2012 , Santin & Eizirik 2013 , Floyel et al. 2015 ). Islets inflammation triggers endoplasmic reticulum (ER) stress in beta cells exacerbating inflammation and contributing to beta cell

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Sun-Ji Park, Tae-Shin Kim, Choon-Keun Park, Sang-Hee Lee, Jin-Man Kim, Kyu-Sun Lee, In-kyu Lee, Jeen-Woo Park, Mark A Lawson, and Dong-Seok Lee

in ER stress through activation of the unfolded protein response (UPR). The UPR serves to alleviate ER stress, rescue ER homeostasis, and prevent cell death through the induction of ER chaperone expression, reduction of protein synthesis, and

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Long The Nguyen, Sonia Saad, Yi Tan, Carol Pollock, and Hui Chen

( Verfaillie et al . 2010 ). This condition, namely ER stress, subsequently triggers a series of adaptive responses known as unfolded protein response (UPR) to limit protein translation, improve protein-folding capacity, as well as activating autophagy

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Jing Cen, Ernest Sargsyan, Anders Forslund, and Peter Bergsten

-term and decreased insulin secretion after long-term exposure of isolated human islets to elevated levels of palmitate. In addition, we investigated the involvement of various mechanisms such as mitochondrial metabolism, AMPK phosphorylation, ER stress

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Shaoqian Zhao, Wen Liu, Jiqiu Wang, Juan Shi, Yingkai Sun, Weiqing Wang, Guang Ning, Ruixin Liu, and Jie Hong

. muciniphila -supplemented mice and the control group. A. muciniphila supplementation attenuates ER stress in metabolic tissues Recent evidence recapitulates the interaction among fat deposition, inappropriate activation of ER stress and

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Shalinee Dhayal, Francesco P Zummo, Matthew W Anderson, Patricia Thomas, Hannah J Welters, Catherine Arden, and Noel G Morgan

regulation of endoplasmic reticulum (ER) stress, where it has been shown that palmitoleate causes a reduction in the expression of pro-apoptotic transcription factors, such as ATF4 and CHOP, in cells treated with palmitate ( Diakogiannaki et al. 2008

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Penny Ahlstrom, Esther Rai, Suharto Chakma, Hee Ho Cho, Palanivel Rengasamy, and Gary Sweeney

2 diabetes and upon aging ( Zhang et al. 2016 , Moller et al. 2017 , Zhou et al. 2017 ). Until recently, the causative role of ER stress in promoting insulin resistance in skeletal muscle was much less studied than other tissues. However

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Sumaira Z Hasnain, Johannes B Prins, and Michael A McGuckin

reticulum (ER) stress in β-cell dysfunction in T2D. We first overview insulin biosynthesis and secretion, summarise the features of progression of diabetes. We then detail the significance of oxidative and ER stress in β-cell homeostasis and dysfunction