ArticlePloS one2014
Dystropathology increases energy expenditure and protein turnover in the mdx mouse model of duchenne muscular dystrophy.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
- Trial
- GDF5 modulation of MuSC pool as a potential therapeutic benefit for DMD.Molecular therapy. Nucleic acids · 2026Article
- A high-fat, high-sucrose diet exacerbates muscle and metabolic pathology and undermines glucocorticoid efficacy in dystrophin-deficient mice.The Journal of physiology · 2026Article
- Longevity of cardiac and skeletal muscle proteins is dependent on tissue and subcellular compartmentation patterns.Cell reports · 2026Article
- Unraveling the link between resting metabolic rate and phase angle in facioscapulohumeral dystrophy: a comparative and associative analysis.European journal of applied physiology · 2025Article
- APE1/Ref-1 inhibition via APX3330 lowers monocyte/macrophage infiltration without ameliorating the structure and function of dystrophic mdx hindlimb muscles.Physiological reports · 2025Article
- Repurposed Nrf2 activator dimethyl fumarate rescues muscle inflammation and fibrosis in an aggravated mdx mouse model of Duchenne muscular dystrophy.Redox biology · 2025Article
- Understanding Duchenne muscular dystrophy-associated brain pathology.Disease models & mechanisms · 2025Review
- Article
- Pharmacology and macrophage modulation of HPGDS inhibitor PK007 demonstrate reduced disease severity in DMD-affected muscles of the mdx mouse model.Skeletal muscle · 2025Article
- A fat- and sucrose-enriched diet causes metabolic alterations in mdx mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
- Biomarkers for Duchenne muscular dystrophy progression: impact of age in the mdx tongue spared muscle.Research square · 2023Article
- Muscle Pathology in Dystrophic Rats and Zebrafish Is Unresponsive to Taurine Treatment, Compared to theMetabolites · 2023Article
- Considering the Promise of Vamorolone for Treating Duchenne Muscular Dystrophy.Journal of neuromuscular diseases · 2023Article
- Article
- Description of Osmolyte Pathways in MaturingInternational journal of molecular sciences · 2022Article
- Dystrophin Dp71 Subisoforms Localize to the Mitochondria of Human Cells.Life (Basel, Switzerland) · 2021Article
- Brief high fat high sugar diet results in altered energy and fat metabolism during pregnancy in mice.Scientific reports · 2020Article
- Genetic reduction of the extracellular matrix protein versican attenuates inflammatory cell infiltration and improves contractile function in dystrophic mdx diaphragm muscles.Scientific reports · 2020Article
- Biomarkers for Duchenne muscular dystrophy: myonecrosis, inflammation and oxidative stress.Disease models & mechanisms · 2020Review
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6 authors.
Funding
No grant is acknowledged in the PubMed record.
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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