Cargando…
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...
Autores principales: | , , , , , , , |
---|---|
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 |
_version_ | 1782384899801481216 |
---|---|
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. |
format | Online Article Text |
id | pubmed-4530391 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Mary Ann Liebert, Inc. |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT glennthomasc endogenousnutritivesupportaftertraumaticbraininjuryperipherallactateproductionforglucosesupplyviagluconeogenesis AT martinneila endogenousnutritivesupportaftertraumaticbraininjuryperipherallactateproductionforglucosesupplyviagluconeogenesis AT mcarthurdavidl endogenousnutritivesupportaftertraumaticbraininjuryperipherallactateproductionforglucosesupplyviagluconeogenesis AT hovdadavida endogenousnutritivesupportaftertraumaticbraininjuryperipherallactateproductionforglucosesupplyviagluconeogenesis AT vespapaul endogenousnutritivesupportaftertraumaticbraininjuryperipherallactateproductionforglucosesupplyviagluconeogenesis AT johnsonmatthewl endogenousnutritivesupportaftertraumaticbraininjuryperipherallactateproductionforglucosesupplyviagluconeogenesis AT horningmichaela endogenousnutritivesupportaftertraumaticbraininjuryperipherallactateproductionforglucosesupplyviagluconeogenesis AT brooksgeorgea endogenousnutritivesupportaftertraumaticbraininjuryperipherallactateproductionforglucosesupplyviagluconeogenesis |