Lactate Metabolism, Signaling, and Function in Brain Development, Synaptic Plasticity, Angiogenesis, and Neurodegenerative Diseases.
development
dysmetabolism
energy
lactate
neurodegeneration
neuroprotective
synaptic plasticity
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
29 Aug 2023
29 Aug 2023
Historique:
received:
24
07
2023
revised:
21
08
2023
accepted:
25
08
2023
medline:
11
9
2023
pubmed:
9
9
2023
entrez:
9
9
2023
Statut:
epublish
Résumé
Neural tissue requires a great metabolic demand despite negligible intrinsic energy stores. As a result, the central nervous system (CNS) depends upon a continuous influx of metabolic substrates from the blood. Disruption of this process can lead to impairment of neurological functions, loss of consciousness, and coma within minutes. Intricate neurovascular networks permit both spatially and temporally appropriate metabolic substrate delivery. Lactate is the end product of anaerobic or aerobic glycolysis, converted from pyruvate by lactate dehydrogenase-5 (LDH-5). Although abundant in the brain, it was traditionally considered a byproduct or waste of glycolysis. However, recent evidence indicates lactate may be an important energy source as well as a metabolic signaling molecule for the brain and astrocytes-the most abundant glial cell-playing a crucial role in energy delivery, storage, production, and utilization. The astrocyte-neuron lactate-shuttle hypothesis states that lactate, once released into the extracellular space by astrocytes, can be up-taken and metabolized by neurons. This review focuses on this hypothesis, highlighting lactate's emerging role in the brain, with particular emphasis on its role during development, synaptic plasticity, angiogenesis, and disease.
Identifiants
pubmed: 37686202
pii: ijms241713398
doi: 10.3390/ijms241713398
pmc: PMC10487923
pii:
doi:
Substances chimiques
Lactic Acid
33X04XA5AT
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIA NIH HHS
ID : R01 AG045781
Pays : United States
Organisme : NIA NIH HHS
ID : RF1 AG045781
Pays : United States
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