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    Diet-induced obesity mediated by the JNK/DIO2 signal transduction pathway

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    Authors
    Vernia, Santiago
    Cavanagh-Kyros, Julie
    Barrett, Tamera
    Jung, Dae Young
    Kim, Jason K.
    Davis, Roger J.
    UMass Chan Affiliations
    Department of Medicine, Division of Endocrinology, Metabolism, and Diabetes
    Program in Molecular Medicine
    Document Type
    Journal Article
    Publication Date
    2013-11-01
    Keywords
    Animals
    *Diet, High-Fat
    Energy Metabolism
    Feedback, Physiological
    Gene Expression Regulation
    Iodide Peroxidase
    MAP Kinase Signaling System
    Mice
    Obesity
    Pituitary Gland, Anterior
    Thyroid Hormones
    DIO2
    JNK
    obesity
    pituitary gland
    thyroid hormone
    Biochemistry
    Cellular and Molecular Physiology
    Endocrinology
    Molecular Biology
    Molecular Genetics
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    Link to Full Text
    http://dx.doi.org/10.1101/gad.223800.113
    Abstract
    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.
    Source
    Vernia 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
    DOI
    10.1101/gad.223800.113
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/44382
    PubMed ID
    24186979
    Related Resources
    Link to Article in PubMed
    Rights

    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/.

    ae974a485f413a2113503eed53cd6c53
    10.1101/gad.223800.113
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