Diet-induced obesity mediated by the JNK/DIO2 signal transduction pathway
Jung, Dae Young
Kim, Jason K.
Davis, Roger J.
UMass Chan AffiliationsDepartment of Medicine, Division of Endocrinology, Metabolism, and Diabetes
Program in Molecular Medicine
Document TypeJournal Article
Gene Expression Regulation
MAP Kinase Signaling System
Pituitary Gland, Anterior
Cellular and Molecular Physiology
MetadataShow full item record
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.
SourceVernia 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. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/44382
Related ResourcesLink to Article in PubMed
This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 3.0 Unported), as described at http://creativecommons.org/licenses/by-nc/3.0/.