Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes

By Umut Özcan, Qiong Cao, E. Yilmaz, Ann-Hwee Lee, N. Iwakoshi, Esra Özdelen, Gurol Tuncman, Cem Z. Görgün, Laurie H. Glimcher, G. Hotamışlıgil. Science, 2004

3,814 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Surgery

View Paper: https://www.semanticscholar.org/paper/7405e03352f9c7e2b7f5987923d766fc499d6cf9

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Citations in the corpus

Endoplasmic reticulum stress signalling and the pathogenesis of non-alcoholic fatty liver disease. (2018, background): “markers in steatotic livers of genetically obese and high-fat diet (HFD)-fed mice (53) as well as in”
Inflammation and metabolic disorders (2006, background): “JNK is activated upon exposure to cytokines such as TNF-α, as well as by free fatty acids and internal cues such as endoplasmic reticulum stress, all of which might underlie the obesity-induced activit”
Endoplasmic reticulum stress signaling in disease. (2006, background): “For unclear reasons, liver and adipose cells from obese mice show biochemical evidence of ER stress with PERK activation, eIF2 phosphorylation, and BiP induction (139).”
Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training (2013, positive): “support cell-based studies as mice deficient (heterozygous null) in XBP-1 develop glucose intolerance and insulin resistance that is associated with tissue inflammation and impaired insulin signaling (486).”
Inflammatory Mechanisms in the Regulation of Insulin Resistance (2008, background): “ATF6 and X-box binding protein-1 (XBP-1) are critical regulators of ER function and its adaptive responses, as gain- and loss-offunction studies with XPB-1 demonstrated the close interaction with insulin action in vitro and in vivo (83).”
Mitofusin 2 (Mfn2) links mitochondrial and endoplasmic reticulum function with insulin signaling and is essential for normal glucose homeostasis (2012, methodology): “Wild-type or L-KO mice were treated or not treated with TUDCA for 3 wk as reported (31).”
The endoplasmic reticulum and the unfolded protein response. (2007, background): “Mice with heterozygous Xbp1 deletion appear normal but develop insulin resistance when fed a high-fat diet [35].”
Toll-like receptor activation of XBP1 regulates innate immune responses in macrophages (2010, background): “Because some diseases such as atherosclerosis, cystic fibrosis, inflammatory bowel disease and type 2 diabetes are characterized by features of both ER stress and inflammatio”
From acute ER stress to physiological roles of the Unfolded Protein Response (2006, background): “proposed that the UPR initiates activation of JNK1 which subsequently phosphorylates serine residue 307 of the insulin receptor substrate-1 (IRS-1), consequently reducing insulin receptor signaling.(83) Recent work has shown that proteintyrosine phosphatase 1B (PTP-1B) interacts with the IRE1/ XBP1 ”
Integrating Mechanisms for Insulin Resistance: Common Threads and Missing Links (2012, positive): “Activation of the UPR was observed in the livers of leptin-deﬁcient ob/ob mice (Ozcan et al., 2004), suggesting that these pathways may be involved in the pathogenesis of insulin resistance in obese states in rodents as well as in humans (Gregor et al., 2009).”
Adipose Tissue Hypoxia in Obesity and Its Impact on Adipocytokine Dysregulation (2007, background): “Recent studies have reported that ER stress is increased in liver and adipose tissue of obese mice (23,24).”
Adipocytokines: mediators linking adipose tissue, inflammation and immunity (2006, background): “Another important mechanism involved in insulin resistance is endoplasmic-reticulum (ER) stress”