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Endogenous Nutritive Support after Traumatic Brain Injury: Peripheral Lactate Production for Glucose Supply via Gluconeogenesis.
Glenn, Thomas C; Martin, Neil A; McArthur, David L; Hovda, David A; Vespa, Paul; Johnson, Matthew L; Horning, Michael A; Brooks, George A.
Afiliación
  • Glenn TC; 1University of California, Los Angeles, Cerebral Blood Flow Laboratory, Los Angeles, California.
  • Martin NA; 2Division of Neurosurgery, University of California, Los Angeles (UCLA), UCLA Center for Health Sciences, Los Angeles, California.
  • McArthur DL; 1University of California, Los Angeles, Cerebral Blood Flow Laboratory, Los Angeles, California.
  • Hovda DA; 2Division of Neurosurgery, University of California, Los Angeles (UCLA), UCLA Center for Health Sciences, Los Angeles, California.
  • Vespa P; 1University of California, Los Angeles, Cerebral Blood Flow Laboratory, Los Angeles, California.
  • Johnson ML; 1University of California, Los Angeles, Cerebral Blood Flow Laboratory, Los Angeles, California.
  • Horning MA; 1University of California, Los Angeles, Cerebral Blood Flow Laboratory, Los Angeles, California.
  • Brooks GA; 3Department of Integrative Biology, University of California, Berkeley, Berkeley, California.
J Neurotrauma ; 32(11): 811-9, 2015 Jun 01.
Article en En | MEDLINE | ID: mdl-25279664
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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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Lesiones Encefálicas / Estado Nutricional / Ácido Láctico / Gluconeogénesis / Glucosa Tipo de estudio: Diagnostic_studies Límite: Adolescent / Adult / Female / Humans / Male / Middle aged Idioma: En Revista: J Neurotrauma Asunto de la revista: NEUROLOGIA / TRAUMATOLOGIA Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Lesiones Encefálicas / Estado Nutricional / Ácido Láctico / Gluconeogénesis / Glucosa Tipo de estudio: Diagnostic_studies Límite: Adolescent / Adult / Female / Humans / Male / Middle aged Idioma: En Revista: J Neurotrauma Asunto de la revista: NEUROLOGIA / TRAUMATOLOGIA Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos