ArticleCNS neuroscience & therapeutics2018
Altered lactate metabolism in Huntington's disease is dependent on GLUT3 expression.
Article in CNS neuroscience & therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Roles of lactate and protein lactylation in neurogenesis and neurodegenerative disease.Journal of translational medicine · 2026Review
- Glucose transporter 3 gene deficiency modifies Huntington's disease progression in zQ175 model mice.Experimental neurology · 2026Article
- Protein Lactylation in Central Nervous System Diseases: Molecular Mechanisms and Targeted Therapeutic Strategies.International journal of nanomedicine · 2026Review
- Lactate and cognition: a dual modulator.Frontiers in molecular neuroscience · 2026Review
- Lactate Transport via Glial MCT1 and Neuronal MCT2 Is Not Required for Synchronized Synaptic Transmission in Hippocampal Slices Supplied With Glucose.Journal of neurochemistry · 2025Article
- Lactate metabolism in neurodegenerative diseases.Neural regeneration research · 2024Review
- Huntington's Disease Drug Development: A Phase 3 Pipeline Analysis.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Construction of the lactate-sensing fibremats by confining sensor fluorescent protein of lactate inside nanofibers of the poly(HPMA/DAMA)/ADH-nylon 6 core-shell fibremat.RSC advances · 2023Article
- Molecular Pathophysiological Mechanisms in Huntington's Disease.Biomedicines · 2022Review
- Genetically Encoded Fluorescent Biosensors for Biomedical Applications.Biomedicines · 2021Review
- Glucose metabolic crosstalk and regulation in brain function and diseases.Progress in neurobiology · 2021Review
- Ganglioside GM1 Targets Astrocytes to Stimulate Cerebral Energy Metabolism.Frontiers in pharmacology · 2021Article
- Redistribution of Monocarboxylate 1 and 4 in Hippocampus and Spatial Memory Impairment Induced by Long-term Ketamine Administration.Frontiers in behavioral neuroscience · 2020Article
- Transcript Analysis of Zebrafish GLUT3 Genes,Frontiers in molecular neuroscience · 2019Article
- The TinyInternational journal of molecular sciences · 2018Review
- Altered lactate metabolism in Huntington's disease is dependent on GLUT3 expression.CNS neuroscience & therapeutics · 2018Article
- Huntington's disease: From basic science to therapeutics.CNS neuroscience & therapeutics · 2018Article
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsHuntington's disease (HD) is a neurodegenerative disorder characterized by progressive abnormalities in cognitive function, mental state, and motor control. HD is characterized by a failure in brain energy metabolism. It has been proposed that monocarboxylates, such as lactate, support brain activity. During neuronal synaptic activity, ascorbic acid released from glial cells stimulates lactate and inhibits glucose transport. The aim of this study was to evaluate the expression and function of monocarboxylate transporters (MCTs) in two HD models.
methodsUsing immunofluorescence, qPCR, and Western blot analyses, we explored mRNA and protein levels of MCTs in the striatum of R6/2 animals and HdhQ7/111 cells. We also evaluated MCT function in HdhQ7/111 cells using radioactive tracers and the fluorescent lactate sensor Laconic.
resultsWe found no significant differences in the mRNA or protein levels of neuronal MCTs. Functional analyses revealed that neuronal MCT2 had a high catalytic efficiency in HD cells. Ascorbic acid did not stimulate lactate uptake in HD cells. Ascorbic acid was also unable to inhibit glucose transport in HD cells because they exhibit decreased expression of the neuronal glucose transporter GLUT3.
conclusionWe demonstrate that stimulation of lactate uptake by ascorbic acid is a consequence of inhibiting glucose transport. Supporting this, lactate transport stimulation by ascorbic acid in HD cells was completely restored by overexpressing GLUT3. Therefore, alterations in GLUT3 expression could be responsible for inefficient use of lactate in HD neurons, contributing to the metabolic failure observed in HD.
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