دورية أكاديمية
أعرض في EDS

Altered skeletal muscle glucose-fatty acid flux in amyotrophic lateral sclerosis.

التفاصيل البيبلوغرافية
العنوان: Altered skeletal muscle glucose-fatty acid flux in amyotrophic lateral sclerosis.
المؤلفون: Steyn FJ; School of Biomedical Sciences, The University of Queensland, St Lucia, Brisbane 4072, Australia.; Centre for Clinical Research, The University of Queensland, Herston, Brisbane 4029, Australia.; Department of Neurology, Royal Brisbane & Women's Hospital, Brisbane 4029, Australia.; Wesley Medical Research, Level 8 East Wing, The Wesley Hospital, Auchenflower 4066, Australia., Li R; School of Biomedical Sciences, The University of Queensland, St Lucia, Brisbane 4072, Australia.; The Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, St Lucia, Brisbane 4072, Australia., Kirk SE; The Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, St Lucia, Brisbane 4072, Australia., Tefera TW; The Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, St Lucia, Brisbane 4072, Australia., Xie TY; School of Biomedical Sciences, The University of Queensland, St Lucia, Brisbane 4072, Australia., Tracey TJ; The Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, St Lucia, Brisbane 4072, Australia., Kelk D; The Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, St Lucia, Brisbane 4072, Australia., Wimberger E; The Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, St Lucia, Brisbane 4072, Australia., Garton FC; Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane 4072, Australia., Roberts L; School of Human Movements and Nutrition Sciences, The University of Queensland, St Lucia, Brisbane 4072, Australia.; School of Allied Health Sciences, Griffith University, Southport, Gold Coast 4222, Australia., Chapman SE; Department of Chemistry and Biochemistry, University of Notre Dame, Notre Dame, IN 46556, USA., Coombes JS; School of Human Movements and Nutrition Sciences, The University of Queensland, St Lucia, Brisbane 4072, Australia., Leevy WM; Department of Chemistry and Biochemistry, University of Notre Dame, Notre Dame, IN 46556, USA., Ferri A; IRCCS Fondazione Santa Lucia, Rome, Italy.; National Research Council, Institute of Translational Pharmacology (IFT), Rome, Italy., Valle C; IRCCS Fondazione Santa Lucia, Rome, Italy.; National Research Council, Institute of Translational Pharmacology (IFT), Rome, Italy., René F; INSERM, U1118, Mécanismes Centraux et Périphériques de la Neurodégénérescence, Strasbourg, France.; Université de Strasbourg, UMRS1118, Strasbourg, France., Loeffler JP; INSERM, U1118, Mécanismes Centraux et Périphériques de la Neurodégénérescence, Strasbourg, France.; Université de Strasbourg, UMRS1118, Strasbourg, France., McCombe PA; Centre for Clinical Research, The University of Queensland, Herston, Brisbane 4029, Australia.; Department of Neurology, Royal Brisbane & Women's Hospital, Brisbane 4029, Australia.; Wesley Medical Research, Level 8 East Wing, The Wesley Hospital, Auchenflower 4066, Australia., Henderson RD; Centre for Clinical Research, The University of Queensland, Herston, Brisbane 4029, Australia.; Department of Neurology, Royal Brisbane & Women's Hospital, Brisbane 4029, Australia.; Wesley Medical Research, Level 8 East Wing, The Wesley Hospital, Auchenflower 4066, Australia., Ngo ST; Centre for Clinical Research, The University of Queensland, Herston, Brisbane 4029, Australia.; Department of Neurology, Royal Brisbane & Women's Hospital, Brisbane 4029, Australia.; Wesley Medical Research, Level 8 East Wing, The Wesley Hospital, Auchenflower 4066, Australia.; The Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, St Lucia, Brisbane 4072, Australia.; Queensland Brain Institute, The University of Queensland, St Lucia, Brisbane 4072, Australia.
المصدر: Brain communications [Brain Commun] 2020 Sep 24; Vol. 2 (2), pp. fcaa154. Date of Electronic Publication: 2020 Sep 24 (Print Publication: 2020).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Oxford University Press Country of Publication: England NLM ID: 101755125 Publication Model: eCollection Cited Medium: Internet ISSN: 2632-1297 (Electronic) Linking ISSN: 26321297 NLM ISO Abbreviation: Brain Commun Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Oxford] : Oxford University Press, [2019]-
مستخلص: Amyotrophic lateral sclerosis is characterized by the degeneration of upper and lower motor neurons, yet an increasing number of studies in both mouse models and patients with amyotrophic lateral sclerosis suggest that altered metabolic homeostasis is also a feature of disease. Pre-clinical and clinical studies have shown that modulation of energy balance can be beneficial in amyotrophic lateral sclerosis. However, the capacity to target specific metabolic pathways or mechanisms requires detailed understanding of metabolic dysregulation in amyotrophic lateral sclerosis. Here, using the superoxide dismutase 1, glycine to alanine substitution at amino acid 93 (SOD1 G93A ) mouse model of amyotrophic lateral sclerosis, we demonstrate that an increase in whole-body metabolism occurs at a time when glycolytic muscle exhibits an increased dependence on fatty acid oxidation. Using myotubes derived from muscle of amyotrophic lateral sclerosis patients, we also show that increased dependence on fatty acid oxidation is associated with increased whole-body energy expenditure. In the present study, increased fatty acid oxidation was associated with slower disease progression. However, within the patient cohort, there was considerable heterogeneity in whole-body metabolism and fuel oxidation profiles. Thus, future studies that decipher specific metabolic changes at an individual patient level are essential for the development of treatments that aim to target metabolic pathways in amyotrophic lateral sclerosis.
(© The Author(s) (2020). Published by Oxford University Press on behalf of the Guarantors of Brain.)
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فهرسة مساهمة: Keywords: amyotrophic lateral sclerosis; fatty acid oxidation; glucose oxidation; hypermetabolism; skeletal muscle
تواريخ الأحداث: Date Created: 20201126 Latest Revision: 20201127
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC7677608
DOI: 10.1093/braincomms/fcaa154
PMID: 33241210
قاعدة البيانات: MEDLINE
الوصف
تدمد:2632-1297
DOI:10.1093/braincomms/fcaa154