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Endogenous Nutritive Support after Traumatic Brain Injury: Peripheral Lactate Production for Glucose Supply via Gluconeogenesis

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., D(2)-glucose, and [3-(13)C]lactate) techniques involving central venous tr...

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Autores principales: Glenn, Thomas C., Martin, Neil A., McArthur, David L., Hovda, David A., Vespa, Paul, Johnson, Matthew L., Horning, Michael A., Brooks, George A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Mary Ann Liebert, Inc. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4530391/
https://www.ncbi.nlm.nih.gov/pubmed/25279664
http://dx.doi.org/10.1089/neu.2014.3482
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author Glenn, Thomas C.
Martin, Neil A.
McArthur, David L.
Hovda, David A.
Vespa, Paul
Johnson, Matthew L.
Horning, Michael A.
Brooks, George A.
author_facet Glenn, Thomas C.
Martin, Neil A.
McArthur, David L.
Hovda, David A.
Vespa, Paul
Johnson, Matthew L.
Horning, Michael A.
Brooks, George A.
author_sort Glenn, Thomas C.
collection PubMed
description 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., D(2)-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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spelling pubmed-45303912015-09-23 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. J Neurotrauma Original Articles 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., D(2)-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. Mary Ann Liebert, Inc. 2015-06-01 /pmc/articles/PMC4530391/ /pubmed/25279664 http://dx.doi.org/10.1089/neu.2014.3482 Text en © Thomas C. Glenn, Neil A. Martin, David L. McArthur, David A. Hovda, Paul Vespa, Matthew L. Johnson, Michael A. Horning, George A. Brooks 2015; Published by Mary Ann Liebert, Inc. This Open Access article is distributed under the terms of the Creative Commons Attribution Noncommercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
spellingShingle Original Articles
Glenn, Thomas C.
Martin, Neil A.
McArthur, David L.
Hovda, David A.
Vespa, Paul
Johnson, Matthew L.
Horning, Michael A.
Brooks, George A.
Endogenous Nutritive Support after Traumatic Brain Injury: Peripheral Lactate Production for Glucose Supply via Gluconeogenesis
title Endogenous Nutritive Support after Traumatic Brain Injury: Peripheral Lactate Production for Glucose Supply via Gluconeogenesis
title_full Endogenous Nutritive Support after Traumatic Brain Injury: Peripheral Lactate Production for Glucose Supply via Gluconeogenesis
title_fullStr Endogenous Nutritive Support after Traumatic Brain Injury: Peripheral Lactate Production for Glucose Supply via Gluconeogenesis
title_full_unstemmed Endogenous Nutritive Support after Traumatic Brain Injury: Peripheral Lactate Production for Glucose Supply via Gluconeogenesis
title_short Endogenous Nutritive Support after Traumatic Brain Injury: Peripheral Lactate Production for Glucose Supply via Gluconeogenesis
title_sort endogenous nutritive support after traumatic brain injury: peripheral lactate production for glucose supply via gluconeogenesis
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4530391/
https://www.ncbi.nlm.nih.gov/pubmed/25279664
http://dx.doi.org/10.1089/neu.2014.3482
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