ArticleNeuro-degenerative diseases2014
SOD1-G93A mice exhibit muscle-fiber-type-specific decreases in glucose uptake in the absence of whole-body changes in metabolism.
Article in Neuro-degenerative diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 23 citations in OpenAlex.
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- Aberrant evoked calcium signaling and nAChR cluster morphology in aFrontiers in cell and developmental biology · 2024Article
- Nutritional and metabolic factors in amyotrophic lateral sclerosis.Nature reviews. Neurology · 2023Review
- Evidence of Metabolic Dysfunction in Amyotrophic Lateral Sclerosis (ALS) Patients and Animal Models.Biomolecules · 2023Review
- Evidence and Metabolic Implications for a New Non-Canonical Role of Cu-Zn Superoxide Dismutase.International journal of molecular sciences · 2023Article
- Metabolic Profile and Pathological Alterations in the Muscle of Patients with Early-Stage Amyotrophic Lateral Sclerosis.Biomedicines · 2022Article
- Gut- and oral-dysbiosis differentially impact spinal- and bulbar-onset ALS, predicting ALS severity and potentially determining the location of disease onset.BMC neurology · 2022Article
- Metabolic Remodeling in Skeletal Muscle Atrophy as a Therapeutic Target.Metabolites · 2021Review
- Skeletal Muscle Metabolism: Origin or Prognostic Factor for Amyotrophic Lateral Sclerosis (ALS) Development?Cells · 2021Review
- Diaphragm neuromuscular transmission failure in aged rats.Journal of neurophysiology · 2019Article
- Defective daily temperature regulation in a mouse model of amyotrophic lateral sclerosis.Experimental neurology · 2019Article
- Specific Physical Exercise Improves Energetic Metabolism in the Skeletal Muscle of Amyotrophic-Lateral- Sclerosis Mice.Frontiers in molecular neuroscience · 2017Article
- Triheptanoin Protects Motor Neurons and Delays the Onset of Motor Symptoms in a Mouse Model of Amyotrophic Lateral Sclerosis.PloS one · 2016Article
- A metabolic switch toward lipid use in glycolytic muscle is an early pathologic event in a mouse model of amyotrophic lateral sclerosis.EMBO molecular medicine · 2015Article
- The interplay between metabolic homeostasis and neurodegeneration: insights into the neurometabolic nature of amyotrophic lateral sclerosis.Cell regeneration (London, England) · 2015Article
- A(a)LS: Ammonia-induced amyotrophic lateral sclerosis.F1000Research · 2015Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundSkeletal muscles play an important role in systemic glucose homeostasis and are purported to be the origin of the altered metabolic state observed in amyotrophic lateral sclerosis (ALS).
objectiveThe purpose of this study was to evaluate whole-body and muscle-specific glucose metabolism in the SOD1-G93A mouse model of ALS.
methodsWe assessed glucose tolerance in early-, middle-, and late-stage SOD1-G93A and control mice using an intraperitoneal glucose tolerance test. We then measured the respiratory exchange ratio (CO2 production/O2 consumption) as a function of fasting and feeding using indirect calorimetry in a subset of male mice at these time points. Finally, muscles from all mice were harvested to evaluate basal and insulin-stimulated glucose transport in fast- and slow-twitch muscles.
resultsNo changes in systemic glucose clearance were observed in SOD1-G93A mice at any stage, nor were there changes in fasting insulin levels. Indirect calorimetry revealed an increase in the respiratory exchange ratio during the fed state at middle, but not at early or late stages of disease. Middle-stage SOD1-G93A mice exhibited decreased insulin-stimulated glucose uptake in fast-twitch, but not slow-twitch, skeletal muscle. Late-stage SOD1-G93A mice exhibited decreased insulin-stimulated glucose uptake in both fast- and slow-twitch muscle, as well as increased basal (non-insulin-stimulated) glucose uptake.
conclusionsThese results suggest that alterations in muscle metabolism occur in a fiber-type-specific manner in ALS, but do not necessarily lead to whole-body metabolic changes in SOD1-G93A mice.
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