ArticleThe Biochemical journal1994
Defective regulation of energy metabolism in mdx-mouse skeletal muscles.
Article in The Biochemical journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 83 citations in OpenAlex.
- Review
- Complexity of skeletal muscle degeneration: multi-systems pathophysiology and organ crosstalk in dystrophinopathy.Pflugers Archiv : European journal of physiology · 2021Review
- Review
- Skeletal Muscle Mitochondria Dysfunction in Genetic Neuromuscular Disorders with Cardiac Phenotype.International journal of molecular sciences · 2021Review
- Multiomics analysis of the mdx/mTR mouse model of Duchenne muscular dystrophy.Connective tissue research · 2021Article
- Targeting Nrf2 for the treatment of Duchenne Muscular Dystrophy.Redox biology · 2021Review
- DOCK3 is a dosage-sensitive regulator of skeletal muscle and Duchenne muscular dystrophy-associated pathologies.Human molecular genetics · 2020Article
- Transcriptome changes during the initiation and progression of Duchenne muscular dystrophy in Caenorhabditis elegans.Human molecular genetics · 2020Article
- Skeletal muscle: A review of molecular structure and function, in health and disease.Wiley interdisciplinary reviews. Systems biology and medicine · 2020Review
- Mitochondrial Dysfunction Is an Early Consequence of Partial or Complete Dystrophin Loss inFrontiers in physiology · 2020Article
- Metabolomic Analyses Reveal Extensive Progenitor Cell Deficiencies in a Mouse Model of Duchenne Muscular Dystrophy.Metabolites · 2018Article
- Long-Term Morpholino Oligomers in Hexose Elicits Long-Lasting Therapeutic Improvements in mdx Mice.Molecular therapy. Nucleic acids · 2018Article
- Gas chromatography/mass spectrometry based metabolomic study in a murine model of irritable bowel syndrome.World journal of gastroenterology · 2018Article
- Mutations in GMPPB Presenting with Pseudometabolic Myopathy.JIMD reports · 2018Article
- Evidence for ACTN3 as a genetic modifier of Duchenne muscular dystrophy.Nature communications · 2017Article
- Co-expression Network Approach Reveals Functional Similarities among Diseases Affecting Human Skeletal Muscle.Frontiers in physiology · 2017Article
- Glucocorticoids enhance muscle endurance and ameliorate Duchenne muscular dystrophy through a defined metabolic program.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Multi-level omics analysis in a murine model of dystrophin loss and therapeutic restoration.Human molecular genetics · 2015Article
- Article
- Quantitative proteomic analysis reveals metabolic alterations, calcium dysregulation, and increased expression of extracellular matrix proteins in laminin α2 chain-deficient muscle.Molecular & cellular proteomics : MCP · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous finding of a reduced energy metabolism in slow- and fast-twitch skeletal muscle fibres from the murine model of Duchenne muscular dystrophy (the mdx mouse) led us to examine the importance of intracellular glucose availability for a normal energy turnover. To this end, basal and KCl-stimulated (20.9 mM total extracellular K+) rates of glucose uptake (GUP) and heat production were measured in isolated, glucose-incubated (5 mM) soleus and extensor digitorum longus muscles from mdx and control C57B1/10 mice, in the presence and in the absence of insulin (1.7 nM). Under all conditions and for both muscle types, glucose uptake values for mdx and control muscles were similar although heat production was lower in mdx muscles. The marked stimulation of GUP by insulin in both mdx and control muscles had only minor effects on heat production. In contrast, glucose deprivation or inhibition of glycolysis with 2-deoxy-D-glucose (5 mM) significantly decreased heat production in control muscles only, which attenuated, although did not suppress, the difference in basal heat production between mdx and control muscles. Stimulation of heat production by a short-chain fatty acid salt (octanoate, 2 mM) was significantly less marked in mdx than in control muscles. Increased cytoplasmic synthesis of CoA by addition of 5 mM pantothenate (vitamin B5) increased the thermogenic response to glucose more in mdx than in control muscles. We conclude that the low energy turnover in mdx-mouse muscle fibres is not due to a decrease of intracellular glucose availability, but rather to a decreased oxidative utilization of glucose and free fatty acids. We suggest that some enzyme complex of the tricarboxylic acid cycle or inefficiency of CoA transport in the mitochondria could be involved.
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