Blood-Brain Glucose Transfer: Repression in Chronic Hyperglycemia
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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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)
- ORCID
- Gjedde, Albert
- 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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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.
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