Is It Possible to Bypass the Block in Cerebral Glucose Uptake Following TBI with Exogenous Lactate?
- 1Integrative Biology, University of California, Berkeley, CA 94720, USA
Abstract
Background/Objectives: Foundational studies on brain carbohydrate metabolism are reviewed. More recent results on the unique functionality of lactate and the possibility of augmenting cerebral carbohydrate (CHO) uptake with exogenous lactate to supplement glucose for brain fueling are presented. This review of the physiological evidence and preliminary clinical observations on cerebral lactate metabolism is intended to spur clinical trials leading to improved patient outcomes following brain injury. Methods: While glucose is widely recognized as the major brain carbohydrate carbon source, the pathway of degradation involves conversion to lactate that occurs under fully oxygenated conditions. The brain is similar to other tissues in that various energy sources compete for use. For the brain, the alternatives are simpler, being restricted to glucose, lactate and ketone bodies. Although the cerebral metabolic rate of glucose use is diminished following TBI, this limitation may be bypassed in whole or part by supplying lactate as a supplemental brain energy source because uptake is undiminished following TBI. Results: The recognition of preferential lactate over glucose use in other tissues and the realization that exogenous lactate may be used to support brain function, normally and in persons following TBI, may be used to our advantage. Conclusions: The healthy brain is carbohydrate dependent. In healthy individuals and following injury, the capacity to augment lactate over glucose use provides an opportunity to support brain function. The hypothesis of using exogenous lactate is presented as a promising metabolic strategy that requires further controlled clinical evaluation.
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BibTeX
@article{brooks2026possible,
title = {{Is It Possible to Bypass the Block in Cerebral Glucose Uptake Following TBI with Exogenous Lactate?}},
author = {George A. Brooks},
journal = {Metabolites},
year = {2026},
month = oct,
doi = {10.3390/metabo16100800},
url = {https://www.mdpi.com/2218-1989/16/10/800},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Is It Possible to Bypass the Block in Cerebral Glucose Uptake Following TBI with Exogenous Lactate?
AU - George A. Brooks
PY - 2026
DA - 2026/10/21
JO - Metabolites
DO - 10.3390/metabo16100800
UR - https://www.mdpi.com/2218-1989/16/10/800
AB - Background/Objectives: Foundational studies on brain carbohydrate metabolism are reviewed. More recent results on the unique functionality of lactate and the possibility of augmenting cerebral carbohydrate (CHO) uptake with exogenous lactate to supplement glucose for brain fueling are presented. This review of the physiological evidence and preliminary clinical observations on cerebral lactate metabolism is intended to spur clinical trials leading to improved patient outcomes following brain injury. Methods: While glucose is widely recognized as the major brain carbohydrate carbon source, the pathway of degradation involves conversion to lactate that occurs under fully oxygenated conditions. The brain is similar to other tissues in that various energy sources compete for use. For the brain, the alternatives are simpler, being restricted to glucose, lactate and ketone bodies. Although the cerebral metabolic rate of glucose use is diminished following TBI, this limitation may be bypassed in whole or part by supplying lactate as a supplemental brain energy source because uptake is undiminished following TBI. Results: The recognition of preferential lactate over glucose use in other tissues and the realization that exogenous lactate may be used to support brain function, normally and in persons following TBI, may be used to our advantage. Conclusions: The healthy brain is carbohydrate dependent. In healthy individuals and following injury, the capacity to augment lactate over glucose use provides an opportunity to support brain function. The hypothesis of using exogenous lactate is presented as a promising metabolic strategy that requires further controlled clinical evaluation.
SN - 2218-1989
ER -