Author(s): CR Figley
Journal of Neuroscience 31(13): 4768-4770.
Lactate is the metabolic byproduct of glycolysis, a process that, despite being less efficient than the complete oxidation of glucose to carbon dioxide and water, occurs throughout the brain. Glycolytic metabolism increases dramatically in response to ischemic events, but even during periods of sufficient oxygen availability, so-called “aerobic glycolysis” may account for as much as 10–12% of glucose metabolism in the adult human brain (Vaishnavi et al., 2010). Moreover, in addition to resting-state glycolysis and baseline lactate production, brain activity has been shown to significantly increase local lactate concentrations (for review, see Mangia et al., 2009). Although the ANLSH predicts that neurons oxidize lactate, it also acknowledges that they may consume significant amounts of glucose (Pellerin et al., 2007). Notwithstanding that, the prediction that plasma lactate could supply up to 60% of the brain’s oxidative fuel, combined with reports that lactate administration is sufficient to support brain function during hypoglycemia (Boumezbeur et al., 2010, and references therein), implies that neurons are capable of transporting and metabolizing large quantities of lactate in vivo: findings that are consistent with previous in vitro spectroscopy studies showing that cultured neurons might preferentially oxidize lactate as their primary metabolic substrate (for review, see Figley and Stroman, 2011). Therefore, despite a higher nominal affinity for lactate uptake into astrocytes (Gandhi et al., 2009), empirical data suggest that large amounts of lactate are transported into neurons, and that this is not likely to represent a rate-limiting step for the ANLSH.