ReviewFrontiers in cellular neuroscience2018
Impairments in Oxidative Glucose Metabolism in Epilepsy and Metabolic Treatments Thereof.
Review in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Emerging perspectives on mitochondrial dysfunctioning and inflammation in epileptogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Pooled it
- Breath Signatures of Antiseizure Medication Response and Tolerability in Adults With Epilepsy.CNS neuroscience & therapeutics · 2026Observational
- Stable Isotope-Resolved Metabolomics in Elucidating Mitochondrial Metabolic Reprogramming and Therapeutic Targets.Biomedical chromatography : BMC · 2026Review
- Glioma region-specific metabolites associated with patient seizures.Journal of neuro-oncology · 2026Article
- The aging gut-glia-immune axis in alzheimer's disease: microbiome-derived mediators of neuroinflammation and therapeutic innovation.GeroScience · 2026Review
- Targeting Reactive Astrocytes with Flavonoids to Alleviate Neuroinflammation and Promote Synaptic Function.Molecular neurobiology · 2026Review
- APOE4 reduces hippocampal expression of phosphoglycerate kinase 1 and sodium potassium pump to enhance seizure susceptibility in mice.Neurobiology of disease · 2026Article
- Multiomic Analyses Reveal Brainstem Metabolic Changes in a Mouse Model of Dravet Syndrome.Cells · 2025Article
- Temporal Dynamics of tsRNA Regulation Mark an Abrupt Transition After Epileptogenesis.Journal of neurochemistry · 2025Article
- Targeting Multilayered Metabolic Networks in Brain Diseases: Emerging Perspectives on Nanodelivery Strategies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Glutamine Metabolism and Metabolic Profiling Using 7 T CRT-FID MRSI in Focal Epilepsy.European journal of neurology · 2025Article
- Metabolic alterations associated with epileptic seizures detected by NMR spectroscopy.Scientific reports · 2025Article
- Article
- Plasma metabolome reveals altered oxidative stress, inflammation, and amino acid metabolism in dogs with idiopathic epilepsy.Epilepsia · 2025Article
- Treatment-Refractory Epilepsy Alimentary Therapy (TREAT): A canine case study.The Canadian veterinary journal = La revue veterinaire canadienne · 2025Article
- Exploring Gut Microbiota-Targeted Therapies for Canine Idiopathic Epilepsy.International journal of molecular sciences · 2025Review
- Metabolic aspects of genetic ion channel epilepsies.Journal of neurochemistry · 2024Review
- Activation of the 5-HT1A Receptor by Eltoprazine Restores Mitochondrial and Motor Deficits in aInternational journal of molecular sciences · 2024Article
- Towards a better understanding of idiopathic epilepsy through metabolic fingerprinting of cerebrospinal fluid in dogs.Scientific reports · 2024Article
- Identification of gene regulatory networks affected across drug-resistant epilepsies.Nature communications · 2024Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is mounting evidence that oxidative glucose metabolism is impaired in epilepsy and recent work has further characterized the metabolic mechanisms involved. In healthy people eating a traditional diet, including carbohydrates, fats and protein, the major energy substrate in brain is glucose. Cytosolic glucose metabolism generates small amounts of energy, but oxidative glucose metabolism in the mitochondria generates most ATP, in addition to biosynthetic precursors in cells. Energy is crucial for the brain to signal "normally," while loss of energy can contribute to seizure generation by destabilizing membrane potentials and signaling in the chronic epileptic brain. Here we summarize the known biochemical mechanisms that contribute to the disturbance in oxidative glucose metabolism in epilepsy, including decreases in glucose transport, reduced activity of particular steps in the oxidative metabolism of glucose such as pyruvate dehydrogenase activity, and increased anaplerotic need. This knowledge justifies the use of alternative brain fuels as sources of energy, such as ketones, TCA cycle intermediates and precursors as well as even medium chain fatty acids and triheptanoin.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.