Cited by 235Barrier Structure and Function StudiesDrug Transport and Resistance MechanismsIon Transport and Channel Regulation

Blood-Brain Glucose Transfer: Repression in Chronic Hyperglycemia

Gjedde, Albert, Crone, Christian·1981·Science

Abstract

Diabetic patients with increased plasma glucose concentrations may develop cerebral symptoms of hypoglycemia when their plasma glucose is rapidly lowered to normal concentrations. The symptoms may indicate insufficient transport of glucose from blood to brain. In rats with chronic hyperglycemia the maximum glucose transport capacity of the blood-brain barrier decreased from 400 to 290 micromoles per 100 grams per minute. When plasma glucose was lowered to normal values, the glucose transport rate into brain was 20 percent below normal. This suggests that repressive changes of the glucose transport mechanism occur in brain endothelial cells in response to increased plasma glucose.

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Crossref · 10.1126/science.7027439

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22 of 22 references verified0 citation errors · 0 not checkable

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  • In rats with chronic hyperglycemia, the maximum glucose transport capacity of the BBB decreased from 400 to 290 micromoles per 100 grams per minute, and the glucose transport rate in the brain decreased to 20 percent below normal when plasma glucose was lowered to normal values.

    “In rats with chronic hyperglycemia, the maximum glucose transport capacity of the BBB decreased from 400 to 290 micromoles per 100 grams per minute, and the glucose transport rate in the brain decreased to 20 percent below normal when plasma glucose was lowered to normal values [3].”

    From A mathematical model of brain glucose homeostasis (2009) · cites this paper as [3]

  • Repressive adaptation of glucose transport across the BBB occurs in response to chronic hyperglycemia to prevent a rise in brain glucose content.

    “On the other hand, repressive adaptation of glucose transport across the blood-brain-barrier (BBB) occurs in response to chronic hyperglycemia to prevent a rise in brain glucose content [3].”

    From A mathematical model of brain glucose homeostasis (2009) · cites this paper as [3]

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Authors
Gjedde, A., & Crone, C.
Affiliations
University of Copenhagen (DK)
Venue
Science
Published
1981-10-23
Volume
214
Issue
4519
Pages
456-457
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2091625139
Cited by
235
References
22
Citations by year
2025: 1 · 2024: 3 · 2023: 1 · 2022: 2 · 2021: 1 · 2020: 1 · 2018: 3 · 2017: 3 · 2016: 1 · 2015: 1 · 2014: 4 · 2013: 4 · 2012: 4
FWCI
5.41
Type
journal article
Language
en
Open access
closed
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
  • Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
chronic hyperglycemia, glucose transport, blood-brain barrier, brain endothelial cells, plasma glucose, rats
MeSH terms
Animals, Biological Transport, Blood-Brain Barrier, Brain, Diabetes Mellitus, Experimental, Glucose, Hyperglycemia, Insulin, Kinetics, Regional Blood Flow, Rats

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