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    Dystropathology increases energy expenditure and protein turnover in the mdx mouse model of Duchenne muscular dystrophy

    213315_139004_85832_C1_Crabb__published_.pdf (711.3Kb)
    Access Status
    Open access
    Authors
    Crabb, Hannah
    Marini, J.
    Sosa, H.
    Castillo, L.
    Grounds, M.
    Fiorotto, M.
    Date
    2014
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Crabb, H. and Marini, J. and Sosa, H. and Castillo, L. and Grounds, M. and Fiorotto, M. 2014. Dystropathology increases energy expenditure and protein turnover in the mdx mouse model of Duchenne muscular dystrophy. PLoS ONE. 9 (2): pp. 1-13.
    Source Title
    PLoS ONE
    DOI
    10.1371/journal.pone.0089277
    ISSN
    1932-6203
    School
    School of Biomedical Sciences
    Remarks

    This article is published under the Open Access publishing model and distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/ Please refer to the licence to obtain terms for any further reuse or distribution of this work

    URI
    http://hdl.handle.net/20.500.11937/28385
    Collection
    • Curtin Research Publications
    Abstract

    The skeletal muscles in Duchenne muscular dystrophy and the mdx mouse model lack functional dystrophin and undergo repeated bouts of necrosis, regeneration, and growth. These processes have a high metabolic cost. However, the consequences for whole body energy and protein metabolism, and on the dietary requirements for these macronutrients at different stages of the disease, are not well-understood. This study used juvenile (4- to 5- wk-old) and adult (12- to 14-wk-old) male dystrophic C57BL/10ScSn-mdx/J and age-matched C57BL/10ScSn/J control male mice to measure total and resting energy expenditure, food intake, spontaneous activity, body composition, whole body protein turnover, and muscle protein synthesis rates. In juvenile mdx mice that have extensive muscle damage, energy expenditure, muscle protein synthesis, and whole body protein turnover rates were higher than in age-matched controls. Adaptations in food intake and decreased activity were insufficient to meet the increased energy and protein needs of juvenile mdx mice and resulted in stunted growth. In (non-growing) adult mdx mice with less severe dystropathology, energy expenditure, muscle protein synthesis, and whole body protein turnover rates were also higher than in age-matched controls. Food intake was sufficient to meet their protein and energy needs, but insufficient to result in fat deposition. These data show that dystropathology impacts the protein and energy needs of mdx mice and that tailored dietary interventions are necessary to redress this imbalance. If not met, the resultant imbalance blunts growth, and may limit the benefits of therapies designed to protect and repair dystrophic muscles.

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