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Exp Neurol. 2019 Jun;316:74-84. doi: 10.1016/j.expneurol.2019.03.018. Epub 2019 Apr 3.

Metabolic perturbations after pediatric TBI: It's not just about glucose.

Author information

1
Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, United States.
2
Department of Neurology, Children's National Health System, George Washington University, School of Medicine & Health Sciences, Washington, DC 20010, United States.
3
Anesthesiology & Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, United States. Electronic address: sscafid2@jhmi.edu.

Abstract

Improved patient survival following pediatric traumatic brain injury (TBI) has uncovered a currently limited understanding of both the adaptive and maladaptive metabolic perturbations that occur during the acute and long-term phases of recovery. While much is known about the redundancy of metabolic pathways that provide adequate energy and substrates for normal brain growth and development, the field is only beginning to characterize perturbations in these metabolic pathways after pediatric TBI. To date, the majority of studies have focused on dysregulated oxidative glucose metabolism after injury; however, the immature brain is well-equipped to use alternative substrates to fuel energy production, growth, and development. A comprehensive understanding of metabolic changes associated with pediatric TBI cannot be limited to investigations of glucose metabolism alone. All energy substrates used by the brain should be considered in developing nutritional and pharmacological interventions for pediatric head trauma. This review summarizes post-injury changes in brain metabolism of glucose, lipids, ketone bodies, and amino acids with discussion of the therapeutic potential of altering substrate utilization to improve pediatric TBI outcomes.

KEYWORDS:

Amino acids; Brain metabolism; Glucose; Ketones; Lipid; Neurometabolism; Oxidative metabolism; Traumatic brain injury (TBI)

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