A metabolic switch toward lipid use in glycolytic muscle is an early pathologic event in a mouse model of amyotrophic lateral sclerosis.
Identifieur interne : 002E04 ( PubMed/Corpus ); précédent : 002E03; suivant : 002E05A metabolic switch toward lipid use in glycolytic muscle is an early pathologic event in a mouse model of amyotrophic lateral sclerosis.
Auteurs : Lavinia Palamiuc ; Anna Schlagowski ; Shyuan T. Ngo ; Aurelia Vernay ; Sylvie Dirrig-Grosch ; Alexandre Henriques ; Anne-Laurence Boutillier ; Joffrey Zoll ; Andoni Echaniz-Laguna ; Jean-Philippe Loeffler ; Frédérique RenéSource :
- EMBO molecular medicine [ 1757-4684 ] ; 2015.
English descriptors
- KwdEn :
- MESH :
- metabolism : Muscles.
- pathology : Amyotrophic Lateral Sclerosis.
- physiology : Muscles.
- physiopathology : Amyotrophic Lateral Sclerosis.
- Animals, Disease Models, Animal, Glycolysis, Lipid Metabolism, Mice.
Abstract
Amyotrophic lateral sclerosis (ALS) is the most common fatal motor neuron disease in adults. Numerous studies indicate that ALS is a systemic disease that affects whole body physiology and metabolic homeostasis. Using a mouse model of the disease (SOD1(G86R)), we investigated muscle physiology and motor behavior with respect to muscle metabolic capacity. We found that at 65 days of age, an age described as asymptomatic, SOD1(G86R) mice presented with improved endurance capacity associated with an early inhibition in the capacity for glycolytic muscle to use glucose as a source of energy and a switch in fuel preference toward lipids. Indeed, in glycolytic muscles we showed progressive induction of pyruvate dehydrogenase kinase 4 expression. Phosphofructokinase 1 was inhibited, and the expression of lipid handling molecules was increased. This mechanism represents a chronic pathologic alteration in muscle metabolism that is exacerbated with disease progression. Further, inhibition of pyruvate dehydrogenase kinase 4 activity with dichloroacetate delayed symptom onset while improving mitochondrial dysfunction and ameliorating muscle denervation. In this study, we provide the first molecular basis for the particular sensitivity of glycolytic muscles to ALS pathology.
DOI: 10.15252/emmm.201404433
PubMed: 25820275
Links to Exploration step
pubmed:25820275Le document en format XML
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<author><name sortKey="Echaniz Laguna, Andoni" sort="Echaniz Laguna, Andoni" uniqKey="Echaniz Laguna A" first="Andoni" last="Echaniz-Laguna">Andoni Echaniz-Laguna</name>
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</affiliation>
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<term>Disease Models, Animal</term>
<term>Glycolysis</term>
<term>Lipid Metabolism</term>
<term>Mice</term>
<term>Muscles (metabolism)</term>
<term>Muscles (physiology)</term>
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<front><div type="abstract" xml:lang="en">Amyotrophic lateral sclerosis (ALS) is the most common fatal motor neuron disease in adults. Numerous studies indicate that ALS is a systemic disease that affects whole body physiology and metabolic homeostasis. Using a mouse model of the disease (SOD1(G86R)), we investigated muscle physiology and motor behavior with respect to muscle metabolic capacity. We found that at 65 days of age, an age described as asymptomatic, SOD1(G86R) mice presented with improved endurance capacity associated with an early inhibition in the capacity for glycolytic muscle to use glucose as a source of energy and a switch in fuel preference toward lipids. Indeed, in glycolytic muscles we showed progressive induction of pyruvate dehydrogenase kinase 4 expression. Phosphofructokinase 1 was inhibited, and the expression of lipid handling molecules was increased. This mechanism represents a chronic pathologic alteration in muscle metabolism that is exacerbated with disease progression. Further, inhibition of pyruvate dehydrogenase kinase 4 activity with dichloroacetate delayed symptom onset while improving mitochondrial dysfunction and ameliorating muscle denervation. In this study, we provide the first molecular basis for the particular sensitivity of glycolytic muscles to ALS pathology.</div>
</front>
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<Abstract><AbstractText>Amyotrophic lateral sclerosis (ALS) is the most common fatal motor neuron disease in adults. Numerous studies indicate that ALS is a systemic disease that affects whole body physiology and metabolic homeostasis. Using a mouse model of the disease (SOD1(G86R)), we investigated muscle physiology and motor behavior with respect to muscle metabolic capacity. We found that at 65 days of age, an age described as asymptomatic, SOD1(G86R) mice presented with improved endurance capacity associated with an early inhibition in the capacity for glycolytic muscle to use glucose as a source of energy and a switch in fuel preference toward lipids. Indeed, in glycolytic muscles we showed progressive induction of pyruvate dehydrogenase kinase 4 expression. Phosphofructokinase 1 was inhibited, and the expression of lipid handling molecules was increased. This mechanism represents a chronic pathologic alteration in muscle metabolism that is exacerbated with disease progression. Further, inhibition of pyruvate dehydrogenase kinase 4 activity with dichloroacetate delayed symptom onset while improving mitochondrial dysfunction and ameliorating muscle denervation. In this study, we provide the first molecular basis for the particular sensitivity of glycolytic muscles to ALS pathology.</AbstractText>
<CopyrightInformation>© 2015 The Authors. Published under the terms of the CC BY 4.0 license.</CopyrightInformation>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Palamiuc</LastName>
<ForeName>Lavinia</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>INSERM, U1118 Mécanismes Centraux et Périphériques de la Neurodégénérescence, Strasbourg, France Université de Strasbourg UMRS1118, Strasbourg, France.</Affiliation>
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<Author ValidYN="Y"><LastName>Schlagowski</LastName>
<ForeName>Anna</ForeName>
<Initials>A</Initials>
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<Author ValidYN="Y"><LastName>Ngo</LastName>
<ForeName>Shyuan T</ForeName>
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</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Vernay</LastName>
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<Author ValidYN="Y"><LastName>Henriques</LastName>
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<Initials>J</Initials>
<AffiliationInfo><Affiliation>Equipe d'Accueil 3072, Mitochondrie, Stress oxydant et Protection Musculaire, Fédération de Médecine Translationelle de Strasbourg, Université de Strasbourg, Strasbourg, France Service de Physiologie et d'Explorations Fonctionnelles, Pôle de Pathologie Thoracique Hôpitaux Universitaires, CHRU de Strasbourg, Strasbourg, France.</Affiliation>
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<Author ValidYN="Y"><LastName>Echaniz-Laguna</LastName>
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<Initials>A</Initials>
<AffiliationInfo><Affiliation>INSERM, U1118 Mécanismes Centraux et Périphériques de la Neurodégénérescence, Strasbourg, France Université de Strasbourg UMRS1118, Strasbourg, France Département de Neurologie, Hôpital de Hautepierre, Hôpitaux Universitaires de Strasbourg, Strasbourg, France.</Affiliation>
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</AffiliationInfo>
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<AffiliationInfo><Affiliation>INSERM, U1118 Mécanismes Centraux et Périphériques de la Neurodégénérescence, Strasbourg, France Université de Strasbourg UMRS1118, Strasbourg, France loeffler@unistra.fr frederique.rene@unistra.fr.</Affiliation>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000690" MajorTopicYN="N">Amyotrophic Lateral Sclerosis</DescriptorName>
<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
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<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006019" MajorTopicYN="Y">Glycolysis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D050356" MajorTopicYN="Y">Lipid Metabolism</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009132" MajorTopicYN="N">Muscles</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
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<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">amyotrophic lateral sclerosis</Keyword>
<Keyword MajorTopicYN="N">exercise</Keyword>
<Keyword MajorTopicYN="N">glucose</Keyword>
<Keyword MajorTopicYN="N">lipids</Keyword>
<Keyword MajorTopicYN="N">muscle</Keyword>
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