Cited by 348Adipokines, Inflammation, and Metabolic DiseasesNF-κB Signaling PathwaysDiet, Metabolism, and Disease

JNK1 and IKKβ: molecular links between obesity and metabolic dysfunction

Solinas, Giovanni, Karin, Michael·2010·The FASEB Journal

Abstract

Inflammation is thought to underlie the pathogenesis of many chronic diseases. It is now established that obesity results in a state of chronic low‐grade inflammation thought to contribute to several metabolic disorders' including insulin resistance and pancreatic islet dysfunction. The protein kinases JNK1 and IKKβ have been found to serve as critical molecular links between obesity, metabolic inflammation, and disorders of glucose homeostasis. The precise mechanisms of these linkages are still being investigated. However, as we discuss here, JNK1 and IKKβ are activated by almost all forms of metabolic stress that have been implicated in insulin resistance or islet dysfunction. Furthermore, both JNK1 and IKKβ are critically involved in the promotion of diet‐induced obesity, metabolic inflammation, insulin resistance, and β‐cell dysfunction. Understanding the molecular mechanisms by which JNK1 and IKKβ mediate obesity‐induced metabolic stress is likely to be of importance for the development of new treatments for a variety of obesity‐associated diseases.—Solinas, G., Karin, M. JNK1 and IKKβ: molecular links between obesity and metabolic dysfunction. FASEB J . 24, 2596–2611 (2010). www.fasebj.org

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Crossref · 10.1096/fj.09-151340

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179 of 179 references verified0 citation errors · 0 not checkable

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  • During a pathophysiological state, a large and sustained increase in ROS impairs insulin action, through the activation of stress signaling pathways (i.e., MAPK and JNK), contributing to the pathogenesis of diet-induced insulin resistance.

    “On the other hand, during a pathophysiological state, abundant evidence indicates that a large and sustained increase in ROS impairs insulin action, through the activation of stress signaling pathways (*i.e.,* MAPK and JNK) ([85](#B85), [154](#B154)), contributing to the pathogenesis of diet-induced insulin resistance ([67](#B67)).”

    From Mitochondrial fatty acid oxidation in obesity (2013) · cites this paper as [154]

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Authors
Solinas, G., & Karin, M.
Affiliations
  • University of Fribourg (CH)
  • University of California San Diego (US)
Corresponding author
Solinas, Giovanni
Venue
The FASEB Journal
Publisher
Wiley
Published
2010-04-06
Volume
24
Issue
8
Pages
2596-2611
ISSN
  • 0892-6638 (ISSN-L)
  • 1530-6860
OpenAlex
W2127873334
Cited by
347
References
179
Citations by year
2026: 8 · 2025: 12 · 2024: 13 · 2023: 15 · 2022: 18 · 2021: 20 · 2020: 15 · 2019: 28 · 2018: 28 · 2017: 27 · 2016: 29 · 2015: 31 · 2014: 23 · 2013: 32 · 2012: 28
FWCI
2.91
Type
journal article
Language
en
Open access
closed
Locations
  • The FASEB Journal (publishedVersion)
  • PubMed (publishedVersion)
  • reroDoc Digital Library (submittedVersion)
Funders
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (SNF31003A‐118172)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Keywords
JNK1, IKKβ, obesity, metabolic inflammation, insulin resistance, beta-cell dysfunction, pancreatic islets, glucose homeostasis, metabolic stress, diet-induced obesity, low-grade inflammation
MeSH terms
Humans, Inflammation, Metabolic Diseases, Obesity, Mitogen-Activated Protein Kinase 8, I-kappa B Kinase

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