A stress signaling pathway in adipose tissue regulates hepatic insulin resistance.
basic_science · Level V
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- Record sourced from PubMed, PMID 19056984.
- Also identified by DOI 10.1126/science.1160794 and PMC identifier 2643026.
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Abstract
A high-fat diet causes activation of the regulatory protein c-Jun NH2-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.
Medical subject headings
- Adipocytes
- Insulin Resistance
- Liver
- Mitogen-Activated Protein Kinase 8
- Signal Transduction
- Stress, Physiological