ArticleExperimental neurology2020
Alternative substrate metabolism depends on cerebral metabolic state following traumatic brain injury.
Article in Experimental neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
The trial behind it
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
31 citing papers in PubMed, 36 citations in OpenAlex.
- Exogenous lactate infusion (ELI) in traumatic brain injury: higher dose is better?Critical care (London, England) · 2025Trial
- Review of Recent Advances in Implantable Brain-Computer Interfaces for the Restoration of Motor Function in Patients With Paralysis.Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- Feeding the injured brain: nutrients, dose, timing, and monitoring.Intensive care medicine · 2026Review
- The impact of and changes in the oxidative status in the post-injury period following nonpenetrating traumatic brain injuries.The Journal of international medical research · 2026Article
- Administration of ketogenic intervention as a potential treatment during post-traumatic brain injury recovery: a scoping review.Frontiers in nutrition · 2026Review
- Longitudinal Brain Structural, Neurochemical, and Behavioral Changes Following Traumatic Brain Injury in Immature Rat Brain with ALCAR Treatment.Neurochemical research · 2025Article
- Mild Blast Exposure Dysregulates Metabolic Pathways and Correlation Networking as Evident from LC-MS-Based Plasma Profiling.Molecular neurobiology · 2025Article
- Glutamate uptake is transiently compromised in the perilesional cortex following controlled cortical impact.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Metabolomic in severe traumatic brain injury: exploring primary, secondary injuries, diagnosis, and severity.Critical care (London, England) · 2025Article
- The evolving pathophysiology of TBI and the advantages of temporally-guided combination therapies.Neurochemistry international · 2024Review
- The Uncoupling Effect of 17β-Estradiol Underlies the Resilience of Female-Derived Mitochondria to Damage after Experimental TBI.Life (Basel, Switzerland) · 2024Article
- Differences in Volatile Organic Compounds Between Concussed and Non-concussed Division I Athletes.Cureus · 2024Article
- Tracing the path of disruption:CNS neuroscience & therapeutics · 2024Review
- The role of mitochondrial uncoupling in the regulation of mitostasis after traumatic brain injury.Neurochemistry international · 2024Article
- Pathophysiology-Based Management of Secondary Injuries and Insults in TBI.Biomedicines · 2024Review
- Nervous System Response to Neurotrauma: A Narrative Review of Cerebrovascular and Cellular Changes After Neurotrauma.Journal of molecular neuroscience : MN · 2024Review
- Neuroprotection or Sex Bias: A Protective Response to Traumatic Brain Injury in the Females.CNS & neurological disorders drug targets · 2024Review
- A case for seeking sex-specific treatments in Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- High-physiological and supra-physiological 1,2-Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- Sex-based differences of antioxidant enzyme nanoparticle effects following traumatic brain injury.Journal of controlled release : official journal of the Controlled Release Society · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Decreases in energy metabolism following traumatic brain injury (TBI) are attributed to impairment of glycolytic flux and oxidative phosphorylation. Glucose utilization post-TBI is decreased while administration of alternative substrates has been shown to be neuroprotective. Changes in energy metabolism following TBI happens in two phases; a period of hyper-metabolism followed by prolonged hypo-metabolism. It is not understood how different cerebral metabolic states may impact substrate metabolism and ultimately mitochondrial function. Adult male or female Sprague Dawley rats were given sham surgery or controlled cortical impact (CCI) and were assigned one of two administration schemes. Glucose, lactate or beta-hydroxybutyrate (BHB) were infused i.v. either starting immediately after injury or beginning 6 h post-injury for 3 h to reflect the hyper- and hypo-metabolic stages. Animals were euthanized 24 h post-injury. The peri-contusional cortex was collected and assayed for mitochondrial respiration peroxide production, and citrate synthase activity. Tissue acetyl-CoA, ATP, glycogen and HMGB1 were also quantified. Sex differences were observed in injury pattern. Administration based on cerebral metabolic state identified that only early lactate and late BHB improved mitochondrial function and peroxide production and TCA cycle intermediates in males. In contrast, both early and late BHB had deleterious effects on all aspects of metabolic measurements in females. These data stress there is no one optimal alternative substrate, but rather the fuel type used should be guided by both cerebral metabolic state and sex.
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Registered trials
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