Brain lactate metabolism: the discoveries and the controversies.
Level 5 - mechanism / opinion, no new human data
Narrative review of cellular and physiological literature without systematic review methodology.
PubMed 22186669 · doi:10.1038/jcbfm.2011.175
What was done
This narrative review synthesized experimental findings and tabular data from multiple laboratories examining brain lactate transport, cellular glycolysis, and metabolic responses to excitatory neurotransmission across astrocyte cultures, neuronal preparations, synaptosomes, and human physiological studies.
What was found
The abstract reports no numeric values or statistical effect sizes. It reports that glutamate-stimulated glycolysis is not universal across astrocyte cultures; synaptosomes and cultured neurons increase glucose transport, glycolysis, and respiration upon glutamate stimulation; lactate accumulation during brain activation reflects a minor fraction of total glucose metabolism; brain activation with low plasma lactate produces outward brain-to-blood gradients with rapid lactate release; and brain lactate uptake increases during strenuous exercise or exogenous lactate infusions.
Why it matters
It provides critical context to the astrocyte-neuron lactate shuttle debate, concluding that glucose remains the predominant fuel for brain activation under normal conditions, with lactate serving as an opportunistic, glucose-sparing substrate when blood levels rise.
Limits
The review lacks systematic search methods and quantitative meta-analytic pooling. The underlying evidence relies heavily on discordant in vitro preparations (cell cultures and synaptosomes) whose metabolic behaviors may not fully replicate intact human brain physiology.
Cited by
- supports The brain can use lactate as an energy fuel, albeit to lower levels than glucose and ketones.