A central role for JNK in obesity and insulin resistance
By J. Hirosumi, Gurol Tuncman, Lufen Chang, Cem Z. Görgün, K. Uysal, K. Maeda, M. Karin, G. Hotamisligil. Nature, 2002
3,411 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/877b67ffa8eb5d04e36ad36b25e820d7ca0a7127
How researchers see this paper
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In Epidemiology
- G. Hotamışlıgil
- Haiming Cao
- Herbert Tilg
- B. Spiegelman
- Jerrold M. Olefsky
- Mitchell A. Lazar
- R. Kaufman
- A. Moschen
In Molecular Biology
- David M. Sabatini
- G. Hotamışlıgil
- Ralph DeFronzo
- R. Kaufman
- J. Engelman
- B. Spiegelman
- M. Karin
- Lewis C. Cantley
Citations in the corpus
- Integrating Mechanisms for Insulin Resistance: Common Threads and Missing Links (2012, neutral): “However, JNK1 knockout mice gain less weight compared to their wild-type control littermates and had slightly higher body temperatures, implying an increase in energy expenditure (Hirosumi et al., 2002).”
- Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training (2013, positive): “Studies in rodents with inactivating mutations in the upstream kinases associated with these signaling pathways, IKKβ and JNK, have shown remarkable efficacy in preventing diet-induced insulin resistance, restraining obesity, and ameliorating T2D (28, 269).”
- Adipocytokines in Obesity and Metabolic Disease (2014, neutral): “Consistent with these observations, JNK1 knockout mice are protected from obesity and insulin resistance (Hirosumi et al. 2002).”
- High-Fat Diet: Bacteria Interactions Promote Intestinal Inflammation Which Precedes and Correlates with Obesity and Insulin Resistance in Mouse (2010, background): “It has been reported that blocking NF-kB in macrophages or liver attenuated inflammatory gene expression and insulin resistance on HF diet [31], c-Jun amino-terminal kinase 1 (JNK1) knockout mice do not become insulin resistant [32] while blocking JNK improves insulin sensitivity [33].”
- Absence of S6K1 protects against age- and diet-induced obesity while enhancing insulin sensitivity (2004, methodology): “Protein extracts from tissue samples were analysed as describe”
- Adipokines in inflammation and metabolic disease (2011, background): “Thus, SFRP5 deficiency exacerbates obesity-induced adipose tissue inflammation and metabolic dysfunction through activation of JNK1 in adipose tissue, and this is consistent with the previously described role for JNK1 in the regulation of insulin resistance and inflammatio”
- Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes (2020, background): “This effect is tissue specific because Jnk1 deficiency in adipocytes does not affect muscle insulin sensitivity (Hirosumi et al., 2002; Sabio et al., 2008).”
- Targeting the phosphoinositide 3-kinase (PI3K) pathway in cancer (2009, background): “S6K- or JNK-knockout mice show increased insulin sensitivity in response to high-fat diets compared with wild-type mic”
- The Human Obesity Gene Map: The 2005 Update (2006, background): “Acts as an inhibitor of c-Jun N-terminal kinase Reduced adiposity (463,464)”
- Dietary and genetic obesity promote liver inflammation and tumorigenesis by enhancing IL-6 and TNF expression (2010, result): “Consistent with previous findings (Hirosumi et al., 2002; Solinas et al., 2007), obese mice exhibited elevated JNK activity in liver and even a larger increase in JNK phosphorylation in HCCs (Figures 4B and 4C).”
- An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer's disease- associated Aβ oligomers. (2012, neutral): “Previous studies have linked IRS-1 serine phosphorylation to JNK activation in diabetes and in obesity-related insulin resistance (22).”