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dc.contributor.authorVernia, Santiago
dc.contributor.authorCavanagh-Kyros, Julie
dc.contributor.authorBarrett, Tamera
dc.contributor.authorJung, Dae Young
dc.contributor.authorKim, Jason K.
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:10:17.000
dc.date.accessioned2022-08-23T17:03:14Z
dc.date.available2022-08-23T17:03:14Z
dc.date.issued2013-11-01
dc.date.submitted2014-04-14
dc.identifier.citationVernia S, Cavanagh-Kyros J, Barrett T, Jung DY, Kim JK, Davis RJ. Diet-induced obesity mediated by the JNK/DIO2 signal transduction pathway. Genes Dev. 2013 Nov 1;27(21):2345-55. doi: 10.1101/gad.223800.113. <a href="http://dx.doi.org/10.1101/gad.223800.113">Link to article on publisher's site</a>
dc.identifier.issn0890-9369 (Linking)
dc.identifier.doi10.1101/gad.223800.113
dc.identifier.pmid24186979
dc.identifier.urihttp://hdl.handle.net/20.500.14038/44382
dc.description.abstractThe cJun N-terminal kinase (JNK) signaling pathway is a key mediator of metabolic stress responses caused by consuming a high-fat diet, including the development of obesity. To test the role of JNK, we examined diet-induced obesity in mice with targeted ablation of Jnk genes in the anterior pituitary gland. These mice exhibited an increase in the pituitary expression of thyroid-stimulating hormone (TSH), an increase in the blood concentration of thyroid hormone (T4), increased energy expenditure, and markedly reduced obesity compared with control mice. The increased amount of pituitary TSH was caused by reduced expression of type 2 iodothyronine deiodinase (Dio2), a gene that is required for T4-mediated negative feedback regulation of TSH expression. These data establish a molecular mechanism that accounts for the regulation of energy expenditure and the development of obesity by the JNK signaling pathway.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=24186979&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1101/gad.223800.113
dc.rights<p>This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see <a href="http://genesdev.cshlp.org/site/misc/terms.xhtml">http://genesdev.cshlp.org/site/misc/terms.xhtml</a>). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 3.0 Unported), as described at <a href="http://creativecommons.org/licenses/by-nc/3.0/">http://creativecommons.org/licenses/by-nc/3.0/</a>.</p>
dc.subjectAnimals
dc.subject*Diet, High-Fat
dc.subjectEnergy Metabolism
dc.subjectFeedback, Physiological
dc.subjectGene Expression Regulation
dc.subjectIodide Peroxidase
dc.subjectMAP Kinase Signaling System
dc.subjectMice
dc.subjectObesity
dc.subjectPituitary Gland, Anterior
dc.subjectThyroid Hormones
dc.subjectDIO2
dc.subjectJNK
dc.subjectobesity
dc.subjectpituitary gland
dc.subjectthyroid hormone
dc.subjectBiochemistry
dc.subjectCellular and Molecular Physiology
dc.subjectEndocrinology
dc.subjectMolecular Biology
dc.subjectMolecular Genetics
dc.titleDiet-induced obesity mediated by the JNK/DIO2 signal transduction pathway
dc.typeJournal Article
dc.source.journaltitleGenes and development
dc.source.volume27
dc.source.issue21
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1010&amp;context=pmm_pp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/pmm_pp/11
dc.identifier.contextkey5476841
refterms.dateFOA2022-08-23T17:03:14Z
html.description.abstract<p>The cJun N-terminal kinase (JNK) signaling pathway is a key mediator of metabolic stress responses caused by consuming a high-fat diet, including the development of obesity. To test the role of JNK, we examined diet-induced obesity in mice with targeted ablation of Jnk genes in the anterior pituitary gland. These mice exhibited an increase in the pituitary expression of thyroid-stimulating hormone (TSH), an increase in the blood concentration of thyroid hormone (T4), increased energy expenditure, and markedly reduced obesity compared with control mice. The increased amount of pituitary TSH was caused by reduced expression of type 2 iodothyronine deiodinase (Dio2), a gene that is required for T4-mediated negative feedback regulation of TSH expression. These data establish a molecular mechanism that accounts for the regulation of energy expenditure and the development of obesity by the JNK signaling pathway.</p>
dc.identifier.submissionpathpmm_pp/11
dc.contributor.departmentDepartment of Medicine, Division of Endocrinology, Metabolism, and Diabetes
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages2345-55


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