Lack of appropriate stoichiometry: Strong evidence against an energetically important astrocyte-neuron lactate shuttle in brain

Dienel, Gerald A.

doi:10.1002/jnr.24015

Cited by 169Neuroscience and Neuropharmacology ResearchCancer, Hypoxia, and MetabolismAdvanced MRI Techniques and Applications

Lack of appropriate stoichiometry: Strong evidence against an energetically important astrocyte-neuron lactate shuttle in brain

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Dienel, Gerald A.·2017·Journal of Neuroscience Research

DOI 10.1002/jnr.24015

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Abstract

Glutamate‐stimulated aerobic glycolysis in astrocytes coupled with lactate shuttling to neurons where it can be oxidized was proposed as a mechanism to couple excitatory neuronal activity with glucose utilization (CMR glc ) during brain activation. From the outset, this model was not viable because it did not fulfill critical stoichiometric requirements: (i) Calculated glycolytic rates and measured lactate release rates were discordant in cultured astrocytes. (ii) Lactate oxidation requires oxygen consumption, but the oxygen–glucose index (OGI, calculated as CMR O2 /CMR glc ) fell during activation in human brain, and the small rise in CMR O2 could not fully support oxidation of lactate produced by disproportionate increases in CMR glc . (iii) Labeled products of glucose metabolism are not retained in activated rat brain, indicating rapid release of a highly labeled, diffusible metabolite identified as lactate, thereby explaining the CMR glc –CMR O2 mismatch. Additional independent lines of evidence against lactate shuttling include the following: astrocytic oxidation of glutamate after its uptake can help “pay” for its uptake without stimulating glycolysis; blockade of glutamate receptors during activation in vivo prevents upregulation of metabolism and lactate release without impairing glutamate uptake; blockade of β‐adrenergic receptors prevents the fall in OGI in activated human and rat brain while allowing glutamate uptake; and neurons upregulate glucose utilization in vivo and in vitro under many stimulatory conditions. Studies in immature cultured cells are not appropriate models for lactate shuttling in adult brain because of their incomplete development of metabolic capability and astrocyte–neuron interactions. Astrocyte–neuron lactate shuttling does not make large, metabolically significant contributions to energetics of brain activation. © 2017 Wiley Periodicals, Inc.

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MCT and lactate transport contribute to neuronal health and function.
“If an ANLS operates at rest, it could also explain why chronic disruption of MCT, LDH, or glycogenolysis in astrocytes can affect neuronal function (Suzuki et al., 2011; Zhang et al., 2016; Mazuel et al., 2017); these and similar results showing that MCT and lactate transport contribute to neuronal health and function provide evidence for some critical biological role for lactate uptake, but do”
From Fueling thought: Management of glycolysis and oxidative phosphorylation in neuronal metabolism (2018) · cites this paper as Dienel, 2017
There is ample evidence of glutamate oxidation by astrocytes.
“and there is ample evidence of glutamate oxidation by astrocytes (Hertz et al., 2007; Dienel, 2017).”
From Fueling thought: Management of glycolysis and oxidative phosphorylation in neuronal metabolism (2018) · cites this paper as Dienel, 2017

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Dringen R, Hoepken HH, Minich T, Ruedig C. 2007. Pentose phos- phate pathway and NADPH metabolism. In: Gibson GE, Dienel GA, editors. Brain energetics integration of molecular and cellular processes. 3rd ed. Berlin (Germany): Springer-Verlag. p. 41-62.
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Astrocyte-Neuron Lactate Shuttle: Concept, Evidence and Role(s)
Pellerin, L. (2026) · HAL
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A Bird's‐Eye View of Glycolytic Upregulation in Activated Brain: The Major Fate of Lactate Is Release From Activated Tissue, Not Shuttling to Nearby Neurons
Dienel, G. A., Rothman, D. L., & Mangia, S. (2025) · Journal of Neurochemistry · doi:10.1111/jnc.70111 · Cited by 21 · see citing works
Astrocytic energetics during excitatory neurotransmission: What are contributions of glutamate oxidation and glycolysis?
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Authors: Dienel, G. A.
Affiliations: University of New Mexico (US)
Corresponding author: Dienel, Gerald A.
ORCID: Dienel, Gerald A.
Venue: Journal of Neuroscience Research
Publisher: Wiley
Published: 2017-02-02
Volume: 95
Issue: 11
Pages: 2103-2125
ISSN: 0360-4012 (ISSN-L)
1097-4547
DOI: 10.1002/jnr.24015
OpenAlex: W2584889633
Cited by: 168
References: 208
Citations by year: 2026: 11 · 2025: 11 · 2024: 12 · 2023: 18 · 2022: 15 · 2021: 24 · 2020: 12 · 2019: 26 · 2018: 27 · 2017: 12
FWCI: 2.59
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Journal of Neuroscience Research (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced MRI Techniques and Applications
Keywords: astrocyte-neuron lactate shuttle, brain energy metabolism, glucose utilization, lactate oxidation, glutamate uptake, glutamate receptor blockade, beta-adrenergic receptors, brain activation, cultured astrocytes
MeSH terms: Animals, Astrocytes, Brain, Energy Metabolism, Glucose, Glycolysis, Humans, Neurons, Oxygen Consumption, Lactic Acid

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Lack of appropriate stoichiometry: Strong evidence against an energetically important astrocyte-neuron lactate shuttle in brain

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