Blood-brain glucose transfer in the mouse

1993 ◽  
Vol 18 (5) ◽  
pp. 591-597 ◽  
Author(s):  
Eain M. Cornford ◽  
Deborah Young ◽  
James W. Paxton ◽  
Shigeyo Hyman ◽  
Catherine L. Farrell ◽  
...  
Keyword(s):  
Brain Glucose ◽  
Glucose Transfer ◽  
Blood Brain

scholarly journals Regional Blood—Brain Glucose Transfer in the Rat: A Novel Double-Membrane Kinetic Analysis

1986 ◽  
Vol 6 (3) ◽  
pp. 305-314 ◽  
Author(s):  
Vincent J. Cunningham ◽  
Richard J. Hargreaves ◽  
David Pelling ◽  
Stephen R. Moorhouse
Keyword(s):  
Endothelial Cell ◽  
Type I ◽  
Type Ii ◽  
Glucose Content ◽  
Brain Glucose ◽  
Glucose Transfer ◽  
Membrane Pores ◽  
Blood Brain ◽  
Anaesthetized Rats ◽  
Glucose Phosphorylation

Regional blood–brain glucose transfer was studied in pentobarbitone-anaesthetized rats using a programmed intravenous infusion technique that maintained steady levels of unlabeled (up to 55 m M) and tracer d-glucose in the circulating plasma. Regional cerebral blood flow, glucose phosphorylation rate, and tissue glucose content were also measured under comparable conditions. Data were analysed in terms of irreversible Michaelis–Menten kinetics assuming independent influx and efflux (Type I) and reversible Michaelis–Menten kinetics (Type II) across both the luminal and the abluminal membranes of the endothelial cell. The latter analysis corresponds to simple stereospecific membrane pores. The mathematical model allowed for changes in tissue glucose content and back-diffusion of tracer during the experiments. Type I analyses gave Kt values of ∼6.6 m M, whereas those by Type II were consistently lower. Interregional differences were not significant using either scheme. Comparison of Type II with Type I analyses revealed a possible explanation for discrepancies in the estimates of nonsaturable glucose transfer by different methods and highlighted the importance of tissue glucose measurements in studies of unidirectional glucose influx. Since the experimental data may be described equally well by either scheme and some interaction between influx and efflux across the endothelial cell might be expected, consideration of this alternative approach is suggested.

scholarly journals Blood-Brain Glucose Transfer in Alzheimer’s disease: Effect of GLP-1 Analog Treatment

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Michael Gejl ◽  
Birgitte Brock ◽  
Lærke Egefjord ◽  
Kim Vang ◽  
Jørgen Rungby ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Glucose ◽  
Glucose Transfer ◽  
Blood Brain ◽  
Disease Effect

Starvation accelerates blood-brain glucose transfer

1981 ◽  
Vol 112 (2) ◽  
pp. 221-223 ◽  
Author(s):  
T. G. CHRISTENSEN ◽  
N. H. DIEMER ◽  
H. LAURSEN ◽  
A. GJEDDE
Keyword(s):  
Brain Glucose ◽  
Glucose Transfer ◽  
Blood Brain

Blood-brain glucose transfer: repression in chronic hyperglycemia

Science ◽  
1981 ◽  
Vol 214 (4519) ◽  
pp. 456-457 ◽  
Author(s):  
A Gjedde ◽  
C Crone
Keyword(s):  
Brain Glucose ◽  
Glucose Transfer ◽  
Chronic Hyperglycemia ◽  
Blood Brain

scholarly journals Regional Blood—Brain Glucose Transfer and Glucose Utilization in Chronically Hyperglycemic, Diabetic Rats following Acute Glycemic Normalization

1990 ◽  
Vol 10 (6) ◽  
pp. 774-780 ◽  
Author(s):  
D. A. Pelligrino ◽  
M. D. Lipa ◽  
R. F. Albrecht
Keyword(s):  
Plasma Glucose ◽  
Glucose Utilization ◽  
Diabetic Rats ◽  
Normal Range ◽  
Brain Glucose ◽  
Glucose Transfer ◽  
Regional Brain ◽  
Blood Brain ◽  
Control Plasma ◽  
Brain Glucose Utilization

Regional rates of brain glucose utilization (rCMRglc) and glucose influx (rJin), along with regional brain tissue glucose concentrations, were measured in chronically hyperglycemic diabetic (CHD) rats following acute glycemic normalization. These results were compared to those obtained in nondiabetic normoglycemic controls. The diabetic rats were evaluated at 6–8 weeks following i.p. streptozotocin injection. All rats were N2O (70%) sedated, paralyzed, and artificially ventilated for study. Acutely normoglycemic (plasma glucose = 7.9 µmol/ml) CHD rats, compared to control (plasma glucose = 8.5 µmol/ml), demonstrated significantly higher ( p < 0.05) rCMRglc and rJin values in 8 of the 11 regions analyzed. Tissue/plasma glucose concentration ratios were significantly greater than control in 9 of 11 regions. Prior to acute glycemic normalization, rCMRglc values in CHD rats were either unchanged or moderately lower than control. These findings indicate that no blood–brain barrier glucose transport repression is present in CHD rats. In fact, the results suggest an increased transport capacity. The increased rCMRglc observed in the acutely normalized CHD rats may be a manifestation of the “hypoglycemic symptoms” observed in chronically hyperglycemic patients following acute glycemic reductions to the normal range. The present results imply that these symptoms are not related to the presence of a relative cerebral glucopenia, as others have suggested.

scholarly journals Blood-Brain Glucose Transfer in Spreading Depression

1981 ◽  
Vol 37 (4) ◽  
pp. 807-812 ◽  
Author(s):  
Albert Gjedde ◽  
Anker Jón Hansen ◽  
Bjørn Quistorff
Keyword(s):  
Spreading Depression ◽  
Brain Glucose ◽  
Glucose Transfer ◽  
Blood Brain

scholarly journals Glucagon-Like Peptide-1 Inhibits Blood-Brain Glucose Transfer in Humans

Diabetes ◽  
2007 ◽  
Vol 57 (2) ◽  
pp. 325-331 ◽  
Author(s):  
S. Lerche ◽  
B. Brock ◽  
J. Rungby ◽  
H. E. Botker ◽  
N. Moller ◽  
...  
Keyword(s):  
Brain Glucose ◽  
Glucose Transfer ◽  
Blood Brain ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1
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