2008/07/24 by Bjørn Quistorff, Niels H. Secher, Johannes J. van Lieshout · 1 citation
Medicine · Neuroscience · Chemistry · #Anesthesia and Sedative Agents #Diet and metabolism studies #Neuroscience and Neuropharmacology Research #Internal medicine #Endocrinology #Epinephrine #Glucose uptake #Chemistry #Carbohydrate metabolism #Adrenergic receptor #Receptor #Medicine #Insulin
paper · doi:10.1096/fj.08-106104
openalex publication_date 2008/07/24 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/04
The human brain releases a small amount of lactate at rest, and even an increase in arterial blood lactate during anesthesia does not provoke a net cerebral lactate uptake. However, during cerebral activation associated with exercise involving a marked increase in plasma lactate, the brain takes up lactate in proportion to the arterial concentration. Cerebral lactate uptake, together with glucose uptake, is larger than the uptake accounted for by the concomitant O(2) uptake, as reflected by the decrease in cerebral metabolic ratio (CMR) [the cerebral molar uptake ratio O(2)/(glucose+(1/2) lactate)] from a resting value of 6 to <2. The CMR also decreases when plasma lactate is not increased, as during prolonged exercise, cerebral activation associated with mental activity, or exposure to a stressful situation. The CMR decrease is prevented with combined beta(1)- and beta(2)-adrenergic receptor blockade but not with beta(1)-adrenergic blockade alone. Also, CMR decreases in response to epinephrine, suggesting that a beta(2)-adrenergic receptor mechanism enhances glucose and perhaps lactate transport across the blood-brain barrier. The pattern of CMR decrease under various forms of brain activation suggests that lactate may partially replace glucose as a substrate for oxidation. Thus, the notion of the human brain as an obligatory glucose consumer is not without exceptions.