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Cited by 558Metabolism, Diabetes, and CancerNeuroscience and Neuropharmacology ResearchIon Transport and Channel Regulation

Glucose transporters in brain in health and disease

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Koepsell, Hermann·2020·Pflügers Archiv - European Journal of Physiology
DOI 10.1007/s00424-020-02441-xPMC PMC7462931
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Abstract

Energy demand of neurons in brain that is covered by glucose supply from the blood is ensured by glucose transporters in capillaries and brain cells. In brain, the facilitative diffusion glucose transporters GLUT1-6 and GLUT8, and the Na + - d -glucose cotransporters SGLT1 are expressed. The glucose transporters mediate uptake of d -glucose across the blood-brain barrier and delivery of d -glucose to astrocytes and neurons. They are critically involved in regulatory adaptations to varying energy demands in response to differing neuronal activities and glucose supply. In this review, a comprehensive overview about verified and proposed roles of cerebral glucose transporters during health and diseases is presented. Our current knowledge is mainly based on experiments performed in rodents. First, the functional properties of human glucose transporters expressed in brain and their cerebral locations are described. Thereafter, proposed physiological functions of GLUT1, GLUT2, GLUT3, GLUT4, and SGLT1 for energy supply to neurons, glucose sensing, central regulation of glucohomeostasis, and feeding behavior are compiled, and their roles in learning and memory formation are discussed. In addition, diseases are described in which functional changes of cerebral glucose transporters are relevant. These are GLUT1 deficiency syndrome (GLUT1-SD), diabetes mellitus, Alzheimer’s disease (AD), stroke, and traumatic brain injury (TBI). GLUT1-SD is caused by defect mutations in GLUT1. Diabetes and AD are associated with changed expression of glucose transporters in brain, and transporter-related energy deficiency of neurons may contribute to pathogenesis of AD. Stroke and TBI are associated with changes of glucose transporter expression that influence clinical outcome.

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  • Mechanisms underlying hypometabolism are thought to involve impaired glucose transport, dysfunctional insulin signaling, and mitochondrial bioenergetics deficits.

    “The mechanisms underlying hypometabolism remain incompletely understood but are thought to involve impaired glucose transport, dysfunctional insulin signaling, and mitochondrial bioenergetics deficits [70].”

    From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [70]

    The ‘Pathogenesis of AD’ section (page unavailable) links hypometabolism to reduced glucose uptake, possibly from decreased blood-brain-barrier glucose transporters, and discusses insulin resistance as a possible contributor to reduced neuronal GLUT4 activity. The paper does not identify mitochondrial bioenergetic deficits as a mechanism of AD hypometabolism; its discussion of hippocampal mitochondrial dysfunction concerns high-fat-diet-fed rats in the ‘Type 2 diabetes mellitus’ section (page unavailable). (LLM, conf=0.86)

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  • Aβ oligomers can directly interact with glucose transporters, promoting their internalization and reducing surface availability, thereby limiting glucose entry into neurons.

    “Experimental studies indicate that Aβ oligomers can directly interact with glucose transporters, promoting their internalization and reducing surface availability, thereby limiting glucose entry into neurons [70, 71].”

    From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [70]

    The ‘Potential roles of glucose transporters during AD pathogenesis’ section reports that applying Aβ decreased Glut3 incorporation into the plasma membrane of cultured neurons. It also proposes that reduced transporter availability can lower intracellular glucose. The paper does not establish that Aβ oligomers directly bind transporters or cause their internalization; reduced membrane incorporation is not the same as internalization. No page number is provided in our copy. (LLM, conf=0.87)

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Authors
Koepsell, H.
Affiliations
University of Würzburg (DE)
Corresponding author
Koepsell, Hermann
ORCID
Koepsell, Hermann
Venue
Pflügers Archiv - European Journal of Physiology
Publisher
Springer Science and Business Media LLC
Published
2020-08-13
Volume
472
Issue
9
Pages
1299-1343
ISSN
  • 0031-6768 (ISSN-L)
  • 1432-2013
DOI
10.1007/s00424-020-02441-x
PMC
PMC7462931
OpenAlex
W3049305782
Cited by
558
References
32
Citations by year
2026: 90 · 2025: 126 · 2024: 88 · 2023: 95 · 2022: 81 · 2021: 70 · 2020: 8
FWCI
6.20
Type
journal article
Language
en
Open access
Licence
Locations
  • Pflügers Archiv - European Journal of Physiology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Informationszentrum Lebenswissenschaften (ZB MED) (submittedVersion, cc-by)
  • Online Publication Service of Würzburg University (Würzburg University) (submittedVersion, cc-by)
Funders
Julius-Maximilians-Universität Würzburg
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
glucose transporters, brain glucose metabolism, GLUT1, GLUT2, GLUT3, GLUT4, SGLT1, blood-brain barrier, astrocytes, glucose detection, feeding behavior, learning and memory, GLUT1 deficiency syndrome, diabetes mellitus, Alzheimer's disease, stroke, traumatic brain injury
MeSH terms
Alzheimer Disease, Animals, Brain, Carbohydrate Metabolism, Inborn Errors, Diabetes Mellitus, Humans, Monosaccharide Transport Proteins, Glucose Transport Proteins, Facilitative

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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