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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Ting Xiao, Xiuci Liang, Hailan Liu, Feng Zhang, Wen Meng, and Fang Hu
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
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
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
Ilitch Aquino Marcondes-de-Castro, Thamiris Ferreira Oliveira, Renata Spezani, Thatiany Souza Marinho, Luiz Eduardo Macedo Cardoso, Marcia Barbosa Aguila, and Carlos Alberto Mandarim-de-Lacerda
, Spezani & Mandarim-de-Lacerda 2022 ). Obesity and T2D have been linked to the endoplasmic reticulum (ER) stress-induced failure of insulin-producing ( Chen et al. 2022 , Lee & Lee 2022 ), which implies more efforts to develop drugs that alleviate
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
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
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
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
Daiana Araujo Santana-Oliveira, Aline Fernandes-da-Silva, Carolline Santos Miranda, Fabiane Ferreira Martins, Carlos Alberto Mandarim-de-Lacerda, and Vanessa Souza-Mello
phenomenon called whitening ( Kotzbeck et al. 2018 ). Endoplasmic reticulum (ER) stress, a condition triggered by the accumulation of unfolded proteins, precedes adipocyte dysfunction and inhibits browning of s.c. WAT (sWAT). Hence, decreased
