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    Rictor/mTORC2 Loss in the Myf5 Lineage Reprograms Brown Fat Metabolism and Protects Mice against Obesity and Metabolic Disease

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    Cell_Reports_Hung_Rictor_1_s2. ...
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    Authors
    Hung, Chien-Min
    Calejman, Camila Martinez
    Sanchez-Gurmaches, Joan
    Li, Huawei
    Clish, Clary B.
    Hettmer, Simone
    Wagers, Amy J.
    Guertin, David A.
    Student Authors
    Chien-Min Hung
    UMass Chan Affiliations
    Program in Molecular Medicine
    Document Type
    Journal Article
    Publication Date
    2014-07-04
    Keywords
    Biochemistry, Biophysics, and Structural Biology
    Cell and Developmental Biology
    
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    Abstract
    The in vivo functions of mechanistic target of rapamycin complex 2 (mTORC2) and the signaling mechanisms that control brown adipose tissue (BAT) fuel utilization and activity are not well understood. Here, by conditionally deleting Rictor in the Myf5 lineage, we provide in vivo evidence that mTORC2 is dispensable for skeletal muscle development and regeneration but essential for BAT growth. Furthermore, deleting Rictor in Myf5 precursors shifts BAT metabolism to a more oxidative and less lipogenic state and protects mice from obesity and metabolic disease at thermoneutrality. We additionally find that Rictor is required for brown adipocyte differentiation in vitro and that the mechanism specifically requires AKT1 hydrophobic motif phosphorylation but is independent of pan-AKT signaling and is rescued with BMP7. Our findings provide insights into the signaling circuitry that regulates brown adipocytes and could have important implications for developing therapies aimed at increasing energy expenditure as a means to combat human obesity.
    Source

    Hung CM, Calejman CM, Sanchez-Gurmaches J, Li H, Clish CB, Hettmer S, Wagers AJ, Guertin DA. Rictor/mTORC2 Loss in the Myf5 Lineage Reprograms Brown Fat Metabolism and Protects Mice against Obesity and Metabolic Disease. Cell Rep. 2014 Jul 10; 8(1):256-271. doi: 10.1016/j.celrep.2014.06.007. Link to article on publisher's site

    DOI
    10.1016/j.celrep.2014.06.007
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/33332
    PubMed ID
    25001283
    Related Resources
    Link to article in PubMed
    Rights

    Copyright 2014 The Authors. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).

    ae974a485f413a2113503eed53cd6c53
    10.1016/j.celrep.2014.06.007
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