title: Modified hormonal effects on fat metabolism after severe head injury in children.
abstract: Previous studies within our research group have indicated that the hormonal influences on whole body energy expenditure may be modified in severely head-injured children. The aim of this study was to examine plasma concentrations of nonesterified fatty acids (NEFA) and the hormonal and metabolic mediators which influence these to determine whether there is a similarly modified effect on fat metabolism. A total of 64 serial measurements were made in 21 fasting severely head-injured children aged 2-15 y (Glasgow Coma Score < or = 8) who were receiving neurointensive care. Circulating NEFA, ketone bodies, and lactate concentrations were analyzed using microenzymatic or electrochemical techniques. Plasma concentrations of adrenaline and insulin were measured using radioenzymatic and RIA techniques, respectively. Net fat oxidation rates were determined using indirect calorimetry. Plasma NEFA concentrations showed a significant positive relationship with both net fat oxidation rates (p = 0.02) and log ketone body concentrations (p = 0.008), indicating that NEFA concentrations were significantly related with utilization. When compared with reference values for normal resting adults, 59 (92%) adrenaline measurements were elevated, whereas only 8 (12%) NEFA values lay above the reference range. Surprisingly, between children, there was a significant negative relationship between NEFA and adrenaline concentrations, even after allowing for the effects of insulin and lactate (p = 0.015). Both plasma NEFA and adrenaline concentrations were significantly related with Glasgo Coma Score (p = 0.04, p = 0.007, respectively), the most severely injured children having the lowest NEFA and highest adrenaline concentrations. The mechanisms underlying these metabolic changes may be related to the severity of head injury and may involve changes in triglyceride/NEFA cycling and/or peripheral effects on adrenergic receptors. If children are to be treated effectively after trauma, it is important to discover the mechanism of these changes which must reflect a fundamental alteration in metabolism.
authors.affiliation: Department of Child Health, University of Newcastle upon Tyne, United Kingdom.
authors.forename: D S
authors.initials: DS
authors.lastname: Matthews
authors.forename: A
authors.initials: A
authors.lastname: Aynsley-Green
authors.forename: J A
authors.initials: JA
authors.lastname: Eyre
mesh_terms: D000293:Adolescent; D000328:Adult; D002648:Child; D002675:Child, Preschool; D006259:Craniocerebral Trauma / Q000097:blood / Q000378:metabolism*; D004837:Epinephrine / Q000097:blood*; D005223:Fats / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood*; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood*; D007657:Ketone Bodies / Q000097:blood; D008297:Male; D010084:Oxidation-Reduction
chemical_list: D005223:Fats; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D007657:Ketone Bodies; D004837:Epinephrine