ArticleJournal of neurotrauma2015
Endogenous Nutritive Support after Traumatic Brain Injury: Peripheral Lactate Production for Glucose Supply via Gluconeogenesis.
Article in Journal of neurotrauma, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02776488 (Exogenous Sodium Lactate Infusion in Traumatic Brain Injury), which is not on this map. Cited by 37 papers.
What it found
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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.
Exogenous Sodium Lactate Infusion in Traumatic Brain Injury (ELI-TBI)
Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- Improvement of Neuroenergetics by Hypertonic Lactate Therapy in Patients with Traumatic Brain Injury Is Dependent on Baseline Cerebral Lactate/Pyruvate Ratio.Journal of neurotrauma · 2016Trial
- Association between lactate-to-albumin ratio and the short-time mortality of patients with ischemic stroke in intensive care unit.BMC neurology · 2026Article
- Molecular vehicles for therapeutic delivery of lactate in exercise and medicine.Sports medicine and health science · 2026Review
- Time-weighted lactate and glucose-lactate ratio outperform static values in ICU mortality prediction after traumatic brain injury: a retrospective cohort study.Journal of intensive care · 2026Article
- Unlocking the metabolic and anti-inflammatory therapeutic potential of lactate in critically ill patients.Critical care (London, England) · 2025Review
- Single-Cell RNA and Transcriptome Sequencing to Analyze the Role of Lactate Metabolism in Traumatic Brain Injury Astrocytes.Brain and behavior · 2025Article
- Altered glucose kinetics occurs with aging: a new outlook on metabolic flexibility.American journal of physiology. Endocrinology and metabolism · 2024Article
- Mitigating Traumatic Brain Injury: A Narrative Review of Supplementation and Dietary Protocols.Nutrients · 2024Review
- Tracing the path of disruption:CNS neuroscience & therapeutics · 2024Review
- Cerebral Glucose Metabolism following TBI: Changes in Plasma Glucose, Glucose Transport and Alternative Pathways of Glycolysis-A Translational Narrative Review.International journal of molecular sciences · 2024Review
- Underfeeding Alters Brain Tissue Synthesis Rate in a Rat Brain Injury Model.International journal of molecular sciences · 2023Article
- Lactate as a myokine and exerkine: drivers and signals of physiology and metabolism.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Review
- Exogenous L-lactate administration in rat hippocampus increases expression of key regulators of mitochondrial biogenesis and antioxidant defense.Frontiers in molecular neuroscience · 2023Article
- Fractional Gluconeogenesis: A Biomarker of Dietary Energy Adequacy in a Rat Brain Injury Model.Metabolites · 2022Article
- Tracing the lactate shuttle to the mitochondrial reticulum.Experimental & molecular medicine · 2022Review
- Lactate in contemporary biology: a phoenix risen.The Journal of physiology · 2022Article
- Lactate Is Answerable for Brain Function and Treating Brain Diseases: Energy Substrates and Signal Molecule.Frontiers in nutrition · 2022Review
- The blood lactate/pyruvate equilibrium affair.American journal of physiology. Endocrinology and metabolism · 2022Article
- Role of the Heart in Lactate Shuttling.Frontiers in nutrition · 2021Review
- The tortuous path of lactate shuttle discovery: From cinders and boards to the lab and ICU.Journal of sport and health science · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
We evaluated the hypothesis that nutritive needs of injured brains are supported by large and coordinated increases in lactate shuttling throughout the body. To that end, we used dual isotope tracer ([6,6-(2)H2]glucose, i.e., D2-glucose, and [3-(13)C]lactate) techniques involving central venous tracer infusion along with cerebral (arterial [art] and jugular bulb [JB]) blood sampling. Patients with traumatic brain injury (TBI) who had nonpenetrating head injuries (n=12, all male) were entered into the study after consent of patients' legal representatives. Written and informed consent was obtained from healthy controls (n=6, including one female). As in previous investigations, the cerebral metabolic rate (CMR) for glucose was suppressed after TBI. Near normal arterial glucose and lactate levels in patients studied 5.7±2.2 days (range of days 2-10) post-injury, however, belied a 71% increase in systemic lactate production, compared with control, that was largely cleared by greater (hepatic+renal) glucose production. After TBI, gluconeogenesis from lactate clearance accounted for 67.1% of glucose rate of appearance (Ra), which was compared with 15.2% in healthy controls. We conclude that elevations in blood glucose concentration after TBI result from a massive mobilization of lactate from corporeal glycogen reserves. This previously unrecognized mobilization of lactate subserves hepatic and renal gluconeogenesis. As such, a lactate shuttle mechanism indirectly makes substrate available for the body and its essential organs, including the brain, after trauma. In addition, when elevations in arterial lactate concentration occur after TBI, lactate shuttling may provide substrate directly to vital organs of the body, including the injured brain.
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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.