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Cited by 604Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismDiet, Metabolism, and Disease

A Stress Signaling Pathway in Adipose Tissue Regulates Hepatic Insulin Resistance

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Sabio, Guadalupe, Das, Madhumita, Mora, Alfonso, Zhang, Zhiyou, Jun, John Y., Ko, Hwi Jin, Barrett, Tamera, Kim, Jason K. +1 more·2008·Science
DOI 10.1126/science.1160794PMC PMC2643026
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Abstract

A high-fat diet causes activation of the regulatory protein c-Jun NH 2 -terminal kinase 1 (JNK1) and triggers development of insulin resistance. JNK1 is therefore a potential target for therapeutic treatment of metabolic syndrome. We explored the mechanism of JNK1 signaling by engineering mice in which the Jnk1 gene was ablated selectively in adipose tissue. JNK1 deficiency in adipose tissue suppressed high-fat diet–induced insulin resistance in the liver. JNK1-dependent secretion of the inflammatory cytokine interleukin-6 by adipose tissue caused increased expression of liver SOCS3, a protein that induces hepatic insulin resistance. Thus, JNK1 activation in adipose tissue can cause insulin resistance in the liver.

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Authors
Sabio, G., Das, M., Mora, A., Zhang, Z., Jun, J. Y., Ko, H. J., Barrett, T., Kim, J. K., & Davis, R. J.
Affiliations
Pennsylvania State University (US)
Corresponding author
Davis, Roger J.
ORCID
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
2008-12-05
Volume
322
Issue
5907
Pages
1539-1543
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
DOI
10.1126/science.1160794
PMC
PMC2643026
OpenAlex
W1993418845
Cited by
604
References
28
Citations by year
2026: 15 · 2025: 26 · 2024: 16 · 2023: 30 · 2022: 23 · 2021: 27 · 2020: 34 · 2019: 22 · 2018: 26 · 2017: 31 · 2016: 41 · 2015: 33 · 2014: 40 · 2013: 49 · 2012: 47
FWCI
35.38
Type
journal article
Language
en
Open access
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
Funders
  • Howard Hughes Medical Institute
  • National Cancer Institute (R01CA065861)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK-52530, R01DK080756, R01DK052530)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Keywords
JNK1, hepatic insulin resistance, adipose tissue, high-fat diet, interleukin-6, SOCS3, metabolic syndrome, inflammatory cytokines
MeSH terms
Suppressor of Cytokine Signaling 3 Protein, Adipose Tissue, Animals, Dietary Fats, Enzyme Activation, Glucose, Insulin, Insulin Resistance, Liver, Phosphorylation, Stress, Physiological, Signal Transduction, Interleukin-6, Adipocytes, MAP Kinase Signaling System, Mitogen-Activated Protein Kinase 8, Suppressor of Cytokine Signaling Proteins, Proto-Oncogene Proteins c-akt, Mice, Insulin Receptor Substrate Proteins

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