D‐ and L‐Amino Acid Blood Concentrations Are Affected in Children With Duchenne Muscular Dystrophy
ABSTRACT Duchenne muscular dystrophy (DMD) is an X‐linked disease caused by the absence of functional dystrophin in the muscle cells. Recent untargeted metabolomics studies identified amino acid metabolism alterations as biochemical pathways potentially involved in DMD pathogenesis. Here, in a well‐...
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| Published in | Journal of cellular and molecular medicine Vol. 29; no. 9; pp. e70495 - n/a |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley & Sons, Inc
01.05.2025
John Wiley and Sons Inc |
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| Online Access | Get full text |
| ISSN | 1582-1838 1582-4934 1582-4934 |
| DOI | 10.1111/jcmm.70495 |
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| Abstract | ABSTRACT
Duchenne muscular dystrophy (DMD) is an X‐linked disease caused by the absence of functional dystrophin in the muscle cells. Recent untargeted metabolomics studies identified amino acid metabolism alterations as biochemical pathways potentially involved in DMD pathogenesis. Here, in a well‐characterised cohort of DMD children and paediatric controls, we investigated by high‐performance liquid chromatography (HPLC) the serum profile of a selected pool of amino acids in D‐ and L‐configuration, including L‐glutamate, L‐glutamine, glycine, L‐aspartate, D‐aspartate, L‐asparagine, L‐serine, and D‐serine. These amino acids are known to modulate neurotransmission and to play essential roles in energy and skeletal muscle metabolism. HPLC determinations highlighted a general amino acid deregulation in DMD compared to controls, including lower levels of L‐aspartate, L‐asparagine, D‐serine, L‐glutamine, and glycine and D−/Total serine ratio. In control subjects, we observed a significant positive correlation between L‐glutamine and age, which lacked in affected children. Conversely, in DMD, we observed (i) a negative correlation of L‐glutamate and L‐aspartate with serum creatinine and creatine kinase levels; (ii) a direct correlation of serum L‐glutamine/L‐glutamate ratio with the fat‐free mass index (as determined by dual energy X‐ray absorptiometry) and with specific motor function scores (North Star Ambulatory Assessment); and (iii) no correlations between glucocorticoid treatment or cognitive function and the serum amino acid profile. Our study highlights significant correlations between serum L‐glutamate levels, L‐glutamine/L‐glutamate ratio, and the multidimensional measures of muscle wasting and motor impairment, suggesting that peripheral glutamine‐glutamate metabolism can be a suitable biomarker of disease severity and progression in DMD patients. |
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| AbstractList | ABSTRACT
Duchenne muscular dystrophy (DMD) is an X‐linked disease caused by the absence of functional dystrophin in the muscle cells. Recent untargeted metabolomics studies identified amino acid metabolism alterations as biochemical pathways potentially involved in DMD pathogenesis. Here, in a well‐characterised cohort of DMD children and paediatric controls, we investigated by high‐performance liquid chromatography (HPLC) the serum profile of a selected pool of amino acids in D‐ and L‐configuration, including L‐glutamate, L‐glutamine, glycine, L‐aspartate, D‐aspartate, L‐asparagine, L‐serine, and D‐serine. These amino acids are known to modulate neurotransmission and to play essential roles in energy and skeletal muscle metabolism. HPLC determinations highlighted a general amino acid deregulation in DMD compared to controls, including lower levels of L‐aspartate, L‐asparagine, D‐serine, L‐glutamine, and glycine and D−/Total serine ratio. In control subjects, we observed a significant positive correlation between L‐glutamine and age, which lacked in affected children. Conversely, in DMD, we observed (i) a negative correlation of L‐glutamate and L‐aspartate with serum creatinine and creatine kinase levels; (ii) a direct correlation of serum L‐glutamine/L‐glutamate ratio with the fat‐free mass index (as determined by dual energy X‐ray absorptiometry) and with specific motor function scores (North Star Ambulatory Assessment); and (iii) no correlations between glucocorticoid treatment or cognitive function and the serum amino acid profile. Our study highlights significant correlations between serum L‐glutamate levels, L‐glutamine/L‐glutamate ratio, and the multidimensional measures of muscle wasting and motor impairment, suggesting that peripheral glutamine‐glutamate metabolism can be a suitable biomarker of disease severity and progression in DMD patients. Duchenne muscular dystrophy (DMD) is an X-linked disease caused by the absence of functional dystrophin in the muscle cells. Recent untargeted metabolomics studies identified amino acid metabolism alterations as biochemical pathways potentially involved in DMD pathogenesis. Here, in a well-characterised cohort of DMD children and paediatric controls, we investigated by high-performance liquid chromatography (HPLC) the serum profile of a selected pool of amino acids in D- and L-configuration, including L-glutamate, L-glutamine, glycine, L-aspartate, D-aspartate, L-asparagine, L-serine, and D-serine. These amino acids are known to modulate neurotransmission and to play essential roles in energy and skeletal muscle metabolism. HPLC determinations highlighted a general amino acid deregulation in DMD compared to controls, including lower levels of L-aspartate, L-asparagine, D-serine, L-glutamine, and glycine and D-/Total serine ratio. In control subjects, we observed a significant positive correlation between L-glutamine and age, which lacked in affected children. Conversely, in DMD, we observed (i) a negative correlation of L-glutamate and L-aspartate with serum creatinine and creatine kinase levels; (ii) a direct correlation of serum L-glutamine/L-glutamate ratio with the fat-free mass index (as determined by dual energy X-ray absorptiometry) and with specific motor function scores (North Star Ambulatory Assessment); and (iii) no correlations between glucocorticoid treatment or cognitive function and the serum amino acid profile. Our study highlights significant correlations between serum L-glutamate levels, L-glutamine/L-glutamate ratio, and the multidimensional measures of muscle wasting and motor impairment, suggesting that peripheral glutamine-glutamate metabolism can be a suitable biomarker of disease severity and progression in DMD patients.Duchenne muscular dystrophy (DMD) is an X-linked disease caused by the absence of functional dystrophin in the muscle cells. Recent untargeted metabolomics studies identified amino acid metabolism alterations as biochemical pathways potentially involved in DMD pathogenesis. Here, in a well-characterised cohort of DMD children and paediatric controls, we investigated by high-performance liquid chromatography (HPLC) the serum profile of a selected pool of amino acids in D- and L-configuration, including L-glutamate, L-glutamine, glycine, L-aspartate, D-aspartate, L-asparagine, L-serine, and D-serine. These amino acids are known to modulate neurotransmission and to play essential roles in energy and skeletal muscle metabolism. HPLC determinations highlighted a general amino acid deregulation in DMD compared to controls, including lower levels of L-aspartate, L-asparagine, D-serine, L-glutamine, and glycine and D-/Total serine ratio. In control subjects, we observed a significant positive correlation between L-glutamine and age, which lacked in affected children. Conversely, in DMD, we observed (i) a negative correlation of L-glutamate and L-aspartate with serum creatinine and creatine kinase levels; (ii) a direct correlation of serum L-glutamine/L-glutamate ratio with the fat-free mass index (as determined by dual energy X-ray absorptiometry) and with specific motor function scores (North Star Ambulatory Assessment); and (iii) no correlations between glucocorticoid treatment or cognitive function and the serum amino acid profile. Our study highlights significant correlations between serum L-glutamate levels, L-glutamine/L-glutamate ratio, and the multidimensional measures of muscle wasting and motor impairment, suggesting that peripheral glutamine-glutamate metabolism can be a suitable biomarker of disease severity and progression in DMD patients. Duchenne muscular dystrophy (DMD) is an X-linked disease caused by the absence of functional dystrophin in the muscle cells. Recent untargeted metabolomics studies identified amino acid metabolism alterations as biochemical pathways potentially involved in DMD pathogenesis. Here, in a well-characterised cohort of DMD children and paediatric controls, we investigated by high-performance liquid chromatography (HPLC) the serum profile of a selected pool of amino acids in D- and L-configuration, including L-glutamate, L-glutamine, glycine, L-aspartate, D-aspartate, L-asparagine, L-serine, and D-serine. These amino acids are known to modulate neurotransmission and to play essential roles in energy and skeletal muscle metabolism. HPLC determinations highlighted a general amino acid deregulation in DMD compared to controls, including lower levels of L-aspartate, L-asparagine, D-serine, L-glutamine, and glycine and D-/Total serine ratio. In control subjects, we observed a significant positive correlation between L-glutamine and age, which lacked in affected children. Conversely, in DMD, we observed (i) a negative correlation of L-glutamate and L-aspartate with serum creatinine and creatine kinase levels; (ii) a direct correlation of serum L-glutamine/L-glutamate ratio with the fat-free mass index (as determined by dual energy X-ray absorptiometry) and with specific motor function scores (North Star Ambulatory Assessment); and (iii) no correlations between glucocorticoid treatment or cognitive function and the serum amino acid profile. Our study highlights significant correlations between serum L-glutamate levels, L-glutamine/L-glutamate ratio, and the multidimensional measures of muscle wasting and motor impairment, suggesting that peripheral glutamine-glutamate metabolism can be a suitable biomarker of disease severity and progression in DMD patients. Duchenne muscular dystrophy (DMD) is an X‐linked disease caused by the absence of functional dystrophin in the muscle cells. Recent untargeted metabolomics studies identified amino acid metabolism alterations as biochemical pathways potentially involved in DMD pathogenesis. Here, in a well‐characterised cohort of DMD children and paediatric controls, we investigated by high‐performance liquid chromatography (HPLC) the serum profile of a selected pool of amino acids in D‐ and L‐configuration, including L‐glutamate, L‐glutamine, glycine, L‐aspartate, D‐aspartate, L‐asparagine, L‐serine, and D‐serine. These amino acids are known to modulate neurotransmission and to play essential roles in energy and skeletal muscle metabolism. HPLC determinations highlighted a general amino acid deregulation in DMD compared to controls, including lower levels of L‐aspartate, L‐asparagine, D‐serine, L‐glutamine, and glycine and D−/Total serine ratio. In control subjects, we observed a significant positive correlation between L‐glutamine and age, which lacked in affected children. Conversely, in DMD, we observed (i) a negative correlation of L‐glutamate and L‐aspartate with serum creatinine and creatine kinase levels; (ii) a direct correlation of serum L‐glutamine/L‐glutamate ratio with the fat‐free mass index (as determined by dual energy X‐ray absorptiometry) and with specific motor function scores (North Star Ambulatory Assessment); and (iii) no correlations between glucocorticoid treatment or cognitive function and the serum amino acid profile. Our study highlights significant correlations between serum L‐glutamate levels, L‐glutamine/L‐glutamate ratio, and the multidimensional measures of muscle wasting and motor impairment, suggesting that peripheral glutamine‐glutamate metabolism can be a suitable biomarker of disease severity and progression in DMD patients. ABSTRACT Duchenne muscular dystrophy (DMD) is an X‐linked disease caused by the absence of functional dystrophin in the muscle cells. Recent untargeted metabolomics studies identified amino acid metabolism alterations as biochemical pathways potentially involved in DMD pathogenesis. Here, in a well‐characterised cohort of DMD children and paediatric controls, we investigated by high‐performance liquid chromatography (HPLC) the serum profile of a selected pool of amino acids in D‐ and L‐configuration, including L‐glutamate, L‐glutamine, glycine, L‐aspartate, D‐aspartate, L‐asparagine, L‐serine, and D‐serine. These amino acids are known to modulate neurotransmission and to play essential roles in energy and skeletal muscle metabolism. HPLC determinations highlighted a general amino acid deregulation in DMD compared to controls, including lower levels of L‐aspartate, L‐asparagine, D‐serine, L‐glutamine, and glycine and D−/Total serine ratio. In control subjects, we observed a significant positive correlation between L‐glutamine and age, which lacked in affected children. Conversely, in DMD, we observed (i) a negative correlation of L‐glutamate and L‐aspartate with serum creatinine and creatine kinase levels; (ii) a direct correlation of serum L‐glutamine/L‐glutamate ratio with the fat‐free mass index (as determined by dual energy X‐ray absorptiometry) and with specific motor function scores (North Star Ambulatory Assessment); and (iii) no correlations between glucocorticoid treatment or cognitive function and the serum amino acid profile. Our study highlights significant correlations between serum L‐glutamate levels, L‐glutamine/L‐glutamate ratio, and the multidimensional measures of muscle wasting and motor impairment, suggesting that peripheral glutamine‐glutamate metabolism can be a suitable biomarker of disease severity and progression in DMD patients. |
| Author | Usiello, Alessandro Panicucci, Chiara Nuzzo, Tommaso Valente, Enza Maria Bruno, Claudio Imarisio, Alberto Brolatti, Noemi Garofalo, Martina Errico, Francesco De Stefano, Maria Egle |
| AuthorAffiliation | 3 Centre of Translational and Experimental Myology IRCCS Istituto Giannina Gaslini Genoa Italy 8 Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health‐DINOGMI University of Genoa Genoa Italy 6 Department of Biology and Biotechnologies “Charles Darwin” Sapienza University Rome Italy 7 Department of Agricultural Sciences University of Naples “Federico II” Portici Italy 5 Neurogenetics Research Centre IRCCS Mondino Foundation Pavia Italy 1 Department of Environmental, Biological and Pharmaceutical Sciences and Technologies Università Degli Studi Della Campania “Luigi Vanvitelli” Caserta Italy 2 CEINGE Biotecnologie Avanzate Franco Salvatore Naples Italy 4 Department of Molecular Medicine University of Pavia Pavia Italy |
| AuthorAffiliation_xml | – name: 4 Department of Molecular Medicine University of Pavia Pavia Italy – name: 1 Department of Environmental, Biological and Pharmaceutical Sciences and Technologies Università Degli Studi Della Campania “Luigi Vanvitelli” Caserta Italy – name: 8 Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health‐DINOGMI University of Genoa Genoa Italy – name: 3 Centre of Translational and Experimental Myology IRCCS Istituto Giannina Gaslini Genoa Italy – name: 6 Department of Biology and Biotechnologies “Charles Darwin” Sapienza University Rome Italy – name: 7 Department of Agricultural Sciences University of Naples “Federico II” Portici Italy – name: 2 CEINGE Biotecnologie Avanzate Franco Salvatore Naples Italy – name: 5 Neurogenetics Research Centre IRCCS Mondino Foundation Pavia Italy |
| Author_xml | – sequence: 1 givenname: Martina surname: Garofalo fullname: Garofalo, Martina organization: CEINGE Biotecnologie Avanzate Franco Salvatore – sequence: 2 givenname: Chiara surname: Panicucci fullname: Panicucci, Chiara organization: IRCCS Istituto Giannina Gaslini – sequence: 3 givenname: Alberto orcidid: 0000-0002-1206-4170 surname: Imarisio fullname: Imarisio, Alberto organization: IRCCS Mondino Foundation – sequence: 4 givenname: Tommaso surname: Nuzzo fullname: Nuzzo, Tommaso organization: CEINGE Biotecnologie Avanzate Franco Salvatore – sequence: 5 givenname: Noemi surname: Brolatti fullname: Brolatti, Noemi organization: IRCCS Istituto Giannina Gaslini – sequence: 6 givenname: Maria Egle surname: De Stefano fullname: De Stefano, Maria Egle organization: Sapienza University – sequence: 7 givenname: Enza Maria surname: Valente fullname: Valente, Enza Maria organization: IRCCS Mondino Foundation – sequence: 8 givenname: Francesco surname: Errico fullname: Errico, Francesco organization: University of Naples “Federico II” – sequence: 9 givenname: Claudio surname: Bruno fullname: Bruno, Claudio email: claudiobruno@gaslini.org organization: University of Genoa – sequence: 10 givenname: Alessandro surname: Usiello fullname: Usiello, Alessandro email: alessandro.usiello@unicampania.it organization: CEINGE Biotecnologie Avanzate Franco Salvatore |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40329488$$D View this record in MEDLINE/PubMed |
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| DOI | 10.1111/jcmm.70495 |
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| Keywords | D‐serine Duchenne muscular dystrophy amino acids motor dysfunction biomarker serum D‐aspartate glutamate muscle wasting |
| Language | English |
| License | Attribution 2025 The Author(s). Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
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| Notes | This work was partially supported by Ricerca Corrente 2023 to CB. The work of AU and TN is supported by #NEXTGENERATIONEU (NGEU) and funded by the Ministry of University and Research (MUR), National Recovery and Resilience Plan (NRRP), and project MNESYS (PE0000006)—A Multiscale integrated approach to the study of the nervous system in health and disease (DN. 1553 11.10.2022). Funding Martina Garofalo, Chiara Panicucci, and Alberto Imarisio contributed equally to this work and share joint first authorship. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Funding: This work was partially supported by Ricerca Corrente 2023 to CB. The work of AU and TN is supported by #NEXTGENERATIONEU (NGEU) and funded by the Ministry of University and Research (MUR), National Recovery and Resilience Plan (NRRP), and project MNESYS (PE0000006)—A Multiscale integrated approach to the study of the nervous system in health and disease (DN. 1553 11.10.2022). |
| ORCID | 0000-0002-1206-4170 |
| OpenAccessLink | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjcmm.70495 |
| PMID | 40329488 |
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| PublicationDate | May 2025 |
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Duchenne muscular dystrophy (DMD) is an X‐linked disease caused by the absence of functional dystrophin in the muscle cells. Recent untargeted... Duchenne muscular dystrophy (DMD) is an X‐linked disease caused by the absence of functional dystrophin in the muscle cells. Recent untargeted metabolomics... Duchenne muscular dystrophy (DMD) is an X-linked disease caused by the absence of functional dystrophin in the muscle cells. Recent untargeted metabolomics... ABSTRACT Duchenne muscular dystrophy (DMD) is an X‐linked disease caused by the absence of functional dystrophin in the muscle cells. Recent untargeted... |
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| SubjectTerms | Adolescent Ambulatory assessment Amino acids Amino Acids - blood Asparagine Attention deficit hyperactivity disorder biomarker Biomarkers Biomarkers - blood Biosynthesis Body composition Body mass index Case-Control Studies Child Child, Preschool Children Chromatography Chromatography, High Pressure Liquid Cognition & reasoning Cognitive ability Creatine Creatine kinase Creatinine Dual energy X-ray absorptiometry Duchenne muscular dystrophy Duchenne's muscular dystrophy Dystrophin D‐aspartate D‐serine Energy metabolism Enzymes Female glutamate Glutamic Acid - blood Glutamine Glutamine - blood High-performance liquid chromatography Humans Intelligence Kinases Male Metabolism Metabolomics motor dysfunction muscle wasting Muscle, Skeletal - metabolism Muscular dystrophy Muscular Dystrophy, Duchenne - blood Neuropsychology Neurotransmission Original Pathogenesis Pediatrics Serine serum Skeletal muscle |
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| Title | D‐ and L‐Amino Acid Blood Concentrations Are Affected in Children With Duchenne Muscular Dystrophy |
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