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A stress signaling pathway in adipose tissue regulates hepatic insulin resistance

dc.contributor.authorSabio, Guadalupe
dc.contributor.authorDas, Madhumita
dc.contributor.authorMora, Alfonso
dc.contributor.authorZhang, Zhiyou
dc.contributor.authorJun, John Y.
dc.contributor.authorKo, Hwi Jin
dc.contributor.authorBarrett, Tamera
dc.contributor.authorKim, Jason K.
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:09:38.000
dc.date.accessioned2022-08-23T16:38:18Z
dc.date.available2022-08-23T16:38:18Z
dc.date.issued2008-12-05
dc.date.submitted2009-11-13
dc.identifier.citationScience. 2008 Dec 5;322(5907):1539-43. <a href="http://dx.doi.org/10.1126/science.1160794">Link to article on publisher's site</a>
dc.identifier.issn1095-9203 (Electronic)
dc.identifier.doi10.1126/science.1160794
dc.identifier.pmid19056984
dc.identifier.urihttp://hdl.handle.net/20.500.14038/39217
dc.description.abstractA 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.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=19056984&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643026/
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.titleA stress signaling pathway in adipose tissue regulates hepatic insulin resistance
dc.typeJournal Article
dc.source.journaltitleScience (New York, N.Y.)
dc.source.volume322
dc.source.issue5907
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2023
dc.identifier.contextkey1063406
html.description.abstract<p>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.</p>
dc.identifier.submissionpathoapubs/2023
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages1539-43


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