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cJun NH2-terminal kinase 1 (JNK1): roles in metabolic regulation of insulin resistance
Open accessAbstract
The cJun NH(2)-terminal kinase isoform JNK1 is implicated in the mechanism of obesity-induced insulin resistance. Feeding a high-fat diet causes activation of the JNK1 signaling pathway, insulin resistance, and obesity in mice. Germ-line ablation of Jnk1 prevents both diet-induced obesity and insulin resistance. Genetic analysis indicates that the effects of JNK1 on insulin resistance can be separated from effects of JNK1 on obesity. Emerging research indicates that JNK1 plays multiple roles in the regulation of insulin resistance, including altered gene expression, hormone/cytokine production, and lipid metabolism. Together, these studies establish JNK1 as a potential pharmacological target for the development of drugs that might be useful for the treatment of insulin resistance, metabolic syndrome, and type 2 diabetes.
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“JNK causes IR by inducing serine and threonine phosphorylation of IRS and attenuating downstream insulin signaling [68].”
From Sarcopenic obesity, insulin resistance, and their implications in cardiovascular and metabolic consequences (2020) · cites this paper as [68]
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“By analogy with JNK1 activity, IRS1 S307 phosphorylation could also have mixed, tissue-specific effects that are obscured by the standard knock-in approach [166].”
BackgroundSkeletal muscle inflammation and insulin resistance in obesity
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JNK Expression by Macrophages Promotes Obesity-Induced Insulin Resistance and Inflammation
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Self-citation
Metadata
- Authors
- Sabio, G., & Davis, R. J.
- Affiliations
- Consejo Superior de Investigaciones Científicas (ES)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Davis, Roger J.
- Venue
- Trends in Biochemical Sciences
- Publisher
- Elsevier BV
- Published
- 2010-09
- Volume
- 35
- Issue
- 9
- Pages
- 490-496
- ISSN
- 0968-0004 (ISSN-L)
- PMC
- PMC2975251
- OpenAlex
- W2123557018
- Cited by
- 170
- References
- 71
- Citations by year
- 2026: 5 · 2025: 13 · 2024: 10 · 2023: 8 · 2022: 9 · 2021: 6 · 2020: 11 · 2019: 11 · 2018: 7 · 2017: 13 · 2016: 17 · 2015: 12 · 2014: 10 · 2013: 15 · 2012: 15
- FWCI
- 1.42
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Biochemical Sciences (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- Funders
- National Cancer Institute (CA065861, R01CA065861)
- National Institute of Diabetes and Digestive and Kidney Diseases (P01DK080665, P30DK032520, DK080665, P30-DK32520)
- National Institute of Neurological Disorders and Stroke (NS054948, R01NS054948)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Keywords
- JNK1, c-Jun N-terminal kinase, insulin resistance, obesity, high-fat diet, metabolic regulation, lipid metabolism, gene expression regulation, cytokine production, metabolic syndrome, type 2 diabetes, therapeutic target
- MeSH terms
- Animals, Diet, Humans, Insulin Resistance, Obesity, Mitogen-Activated Protein Kinase 8, Insulin-Secreting Cells, Mice
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