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dc.contributor.authorScafidi, Susanna
dc.contributor.authorJernberg, Jennifer
dc.contributor.authorFiskum, Gary
dc.contributor.authorMcKenna, Mary C.
dc.date.accessioned2022-09-15T12:29:48Z
dc.date.available2022-09-15T12:29:48Z
dc.date.issued2022-08-01
dc.identifier.urihttp://hdl.handle.net/10713/19801
dc.descriptionData are contained within the article.en_US
dc.description.abstractTraumatic brain injury (TBI) is leading cause of morbidity in young children. Acute dysregulation of oxidative glucose metabolism within the first hours after injury is a hallmark of TBI. The developing brain relies on ketones as well as glucose for energy. Thus, the aim of this study was to determine the metabolism of ketones early after TBI injury in the developing brain. Following the controlled cortical impact injury model of TBI, 21-22-day-old rats were infused with [2,4-13C]β-hydroxybutyrate during the acute (4 h) period after injury. Using ex vivo 13C-NMR spectroscopy, we determined that 13C-β-hydroxybutyrate (13C-BHB) metabolism was increased in both the ipsilateral and contralateral sides of the brain after TBI. Incorporation of the label was significantly higher in glutamate than glutamine, indicating that 13C-BHB metabolism was higher in neurons than astrocytes in both sham and injured brains. Our results show that (i) ketone metabolism was significantly higher in both the ipsilateral and contralateral sides of the injured brain after TBI; (ii) ketones were extensively metabolized by both astrocytes and neurons, albeit higher in neurons; (iii) the pyruvate recycling pathway determined by incorporation of the label from the metabolism of 13C-BHB into lactate was upregulated in the immature brain after TBI.en_US
dc.description.sponsorshipNational Institute of Neurological Disorders and Strokeen_US
dc.description.urihttps://doi.org/10.3390/metabo12080710
dc.language.isoen_USen_US
dc.publisherMDPIen_US
dc.relation.ispartofMetabolites
dc.subjectdeveloping brainen_US
dc.subjectketone bodiesen_US
dc.subjectmetabolismen_US
dc.subjecttraumatic brain injuryen_US
dc.subjectβ-hydroxybutyrateen_US
dc.titleMetabolism of Exogenous [2,4-13C]β-Hydroxybutyrate following Traumatic Brain Injury in 21-22-Day-Old Rats: An Ex Vivo NMR Studyen_US
dc.typeArticleen_US
dc.identifier.doi10.3390/metabo12080710
dc.source.journaltitleMetabolites
dc.source.journaltitleMetabolites
dc.source.volume12
dc.source.issue8
dc.identifier.journalMetabolites


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