In vivo measurements of brain glucose transport using the reversible Michaelis-Menten model and simultaneous measurements of cerebral blood flow changes during hypoglycemia.

Détails

ID Serval
serval:BIB_98A8F9B9B403
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
In vivo measurements of brain glucose transport using the reversible Michaelis-Menten model and simultaneous measurements of cerebral blood flow changes during hypoglycemia.
Périodique
Journal of Cerebral Blood Flow and Metabolism
Auteur⸱e⸱s
Choi I.Y., Lee S.P., Kim S.G., Gruetter R.
ISSN
0271-678X (Print)
ISSN-L
0271-678X
Statut éditorial
Publié
Date de publication
2001
Volume
21
Numéro
6
Pages
653-663
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.Publication Status: ppublish
Résumé
Glucose is the major substrate that sustains normal brain function. When the brain glucose concentration approaches zero, glucose transport across the blood-brain barrier becomes rate limiting for metabolism during, for example, increased metabolic activity and hypoglycemia. Steady-state brain glucose concentrations in alpha-chloralose anesthetized rats were measured noninvasively as a function of plasma glucose. The relation between brain and plasma glucose was linear at 4.5 to 30 mmol/L plasma glucose, which is consistent with the reversible Michaelis-Menten model. When the model was fitted to the brain glucose measurements, the apparent Michaelis-Menten constant, Kt, was 3.3 +/- 1.0 mmol/L, and the ratio of the maximal transport rate relative to CMRglc, Tmax/CMRglc, was 2.7 +/- 0.1. This Kt is comparable to the authors' previous human data, suggesting that glucose transport kinetics in humans and rats are similar. Cerebral blood flow (CBF) was simultaneously assessed and constant above 2 mmol/L plasma glucose at 73 +/- 6 mL 100 g(-1) min(-1). Extrapolation of the reversible Michaelis-Menten model to hypoglycemia correctly predicted the plasma glucose concentration (2.1 +/- 0.6 mmol/L) at which brain glucose concentrations approached zero. At this point, CBF increased sharply by 57% +/- 22%, suggesting that brain glucose concentration is the signal that triggers defense mechanisms aimed at improving glucose delivery to the brain during hypoglycemia.
Mots-clé
Animals, Biological Transport, Blood Flow Velocity, Blood Glucose/analysis, Blood-Brain Barrier, Brain/blood supply, Brain/metabolism, Brain Chemistry, Glucose/analysis, Glucose/metabolism, Hypoglycemia/physiopathology, Kinetics, Magnetic Resonance Spectroscopy, Male, Rats, Rats, Sprague-Dawley
Pubmed
Web of science
Création de la notice
04/08/2010 15:28
Dernière modification de la notice
20/08/2019 15:00
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