GRP78 expression inhibits insulin and ER stress-induced SREBP-1c activation and reduces hepatic steatosis in mice.

By H. Kammoun, H. Chabanon, I. Hainault, S. Luquet, C. Magnan, T. Koike, P. Ferré, F. Foufelle. Journal of Clinical Investigation, 2009

710 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Surgery

View Paper: https://www.semanticscholar.org/paper/6759b1d3bbbbf54ef1517a1eabaf28fb25134f6d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. C. Hetz
2. R. Kaufman
3. G. Hotamışlıgil
4. Shiyu Wang
5. É. Chevet
6. Gerald I. Shulman
7. F. Foufelle
8. P. Ferré

In Epidemiology

1. C. Hetz
2. R. Kaufman
3. G. Hotamışlıgil
4. Shiyu Wang
5. É. Chevet
6. Gerald I. Shulman
7. Ping Li
8. Suneng Fu

In Surgery

1. C. Hetz
2. R. Kaufman
3. G. Hotamışlıgil
4. Shiyu Wang
5. É. Chevet
6. Gerald I. Shulman
7. F. Foufelle
8. P. Ferré

Citations in the corpus

• Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, neutral): “In a similar vein, overexpression of the ER chaperone Grp78 in the liver of obese mice has beneficial metabolic effects (Kammoun et al., 2009).”
• Non Alcoholic Fatty Liver Disease, Hepatic Insulin Resistance and Type 2 Diabetes (2014, background): “, GRP78/BiP) suppressed activation of the UPR and reduced liver lipid content.(97) This is attributed to a decreased expression in SREBP1c and carbohydrateresponsive element-binding protein (ChREBP), two key transcriptional regulators of lipogenesis.”
• Endoplasmic reticulum stress signalling and the pathogenesis of non-alcoholic fatty liver disease. (2018, background): “Hepatic overexpression of GRP78 improves the UPR dynamics, reducing steatosis associated with obesity (60, 173).”
• Triglyceride metabolism in the liver (2017, neutral): “In obese mice, hepatic induction of the UPR pathway reduces Insig-1 levels and leads to the activation of SREBP, increased expression of lipogenic enzymes and ultimately steatosis (129).”
• Endoplasmic Reticulum Stress in Liver Disease (2010, background): “Over expression of the ER chaperone BiP in obese ob/ob mice led to amelioration of ER stress in the liver [61].”
• The impact of the unfolded protein response on human disease (2012, background): “The cytotoxic effects of CHOP are at least in part through GADD34 because CHOP and GADD34 knockout animals are protected from ER stress–induced tissue damage (Marciniak et al., 2004; Malhotra et al., 2008; Song et al., 2008).”
• Integrating Mechanisms for Insulin Resistance: Common Threads and Missing Links (2012, neutral): “Overexpression of GRP78 can suppress activation of the UPR and, in ob/ob mice, can lead to a reduction in liver lipid content (Kammoun et al., 2009).”
• Hepatic steatosis: a role for de novo lipogenesis and the transcription factor SREBP‐1c (2010, background): “Another explanation for the induction of an ER stress in obese rodents could be that the ER is the place where TGs are synthesized and packaged as membrane-embedded neutral lipid particles thus requiring de novo ER membrane formation [45] which could be sensed like a stress by the ER.”
• Defective Hepatic Autophagy in Obesity Promotes ER Stress and Causes Insulin Resistance (2010, background): “Furthermore, ER stress could also act to ell Metabolism 11, 467–478, June 9, 2010 ª2010 Elsevier Inc. 475 regulate lipogenesis and decrease apoB secretion (Kammoun et al., 2009; Su et al., 2009), both of which could alter hepatic lipid accumulation.”
• Energy Metabolism in the Liver (2014, neutral): “of SREBP-1c in the liver, increasing lipogenesis (106).”
• The interaction of hepatic lipid and glucose metabolism in liver diseases. (2012, background): “Recently, activation of PPARδ has been shown to reduce hepatic lipogenesis by suppression of SREPB-1c [76, 77] in addition to increasing the hepatic glucose catabolism as well as muscular oxidation”