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.

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

Elevated endothelial-cell-stimulating angiogenic factor activity in rodent glycolytic skeletal muscles

1991 ◽  
Vol 81 (2) ◽  
pp. 267-270 ◽  
Author(s):  
R. G. Cooper ◽  
C. M. Taylor ◽  
J. J. Choo ◽  
J. B. Weiss
Keyword(s):  
Endothelial Cell ◽  
Skeletal Muscles ◽  
Extensor Digitorum Longus ◽  
Capillary Density ◽  
Extensor Digitorum ◽  
Angiogenic Factor ◽  
Type I ◽  
Type Ii ◽  
Factor Activity ◽  
Angiogenic Activity

1. Capillary density is greater in skeletal muscles comprised of predominantly oxidative (type I) fibres than in those comprised of mainly glycolytic (type II) fibres. In order to investigate further the angiogenic mechanisms involved in muscle capillarization, endothelial-cellstimulating angiogenic factor activities in various rodent skeletal muscles were compared. 2. Eleven untrained adult male Wistar rats were killed and the predominantly oxidative (type I) muscles, soleus and heart, the predominantly glycolytic (type II) muscle, extensor digitorum longus, and the mixed-fibre muscle, gastrocnemius, were removed. Each sample was separately homogenized and centrifuged and the supernatants were diafiltered to isolate the low-molecular-mass fraction containing endothelial-cell-stimulating angiogenic activity. This was assayed for its ability to activate latent collagenase and was expressed as units, where 1 unit represents the percentage activation of the enzyme h−1 (mg of protein in the supernatant)−1. 3. The results (medians and ranges) demonstrated significantly greater endothelial-cell-stimulating angiogenic factor activity in extensor digitorum longus muscle (2.14 units, 0.62–2.87 units, n = 13) than in soleus (0.82 units, 0.59–1.79 units, n = 15), gastrocnemius (0.34 units, 0.28–0.40 units, n = 4) or heart (0.43 units, 0.16–0.52 units, n = 11) (P< 0.01 for each) muscle. 4. These findings suggest that endothelial-cell-stimulating angiogenic activity in muscle is either inversely or not related to the local capillary density, which may be at or near a maximum in physiologically contracting, predominantly oxidative muscles.

scholarly journals Type II iodothyronine deiodinase protein in chicken choroid plexus: additional perspectives on T3 supply in the avian brain

2004 ◽  
Vol 183 (1) ◽  
pp. 235-241 ◽  
Author(s):  
C H J Verhoelst ◽  
V M Darras ◽  
S A Roelens ◽  
G M Artykbaeva ◽  
S Van der Geyten
Keyword(s):  
Epithelial Cells ◽  
Choroid Plexus ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Type I ◽  
Mrna Levels ◽  
Type Ii ◽  
Iodothyronine Deiodinase ◽  
Blood Brain ◽  
D2 Protein

It is widely accepted that type II iodothyronine deiodinase (D2) is mostly present in the brain, where it maintains the homeostasis of thyroid hormone (TH) levels. Although intensive studies have been performed on activity and mRNA levels of the deiodinases, very little is known about their expression at the protein level due to the lack of specific antisera. The current study reports the production of a specific D2 polyclonal antiserum and its use in the comparison of D2 protein distribution with that of type I (D1) and type III (D3) deiodinase protein in the choroid plexus at the blood–brain barrier level. Immunocytochemistry showed very high D2 protein expression in the choroid plexus, especially in the epithelial cells, whereas the D1 and D3 proteins were absent. Furthermore, dexamethasone treatment led to an up-regulation of the D2 protein in the choroid plexus. The expression of D2 protein in the choroid plexus led to a novel insight into the working mechanism of the uptake and transport of thyroid hormones along the blood–brain barrier in birds. It is hypothesized that D2 allows the prohormone thyroxine (T4) to be converted into the active 3,5,3′-triiodothyronine (T3). Within the choroidal epithelial cells. T3 is subsequently bound to its carrier protein, transthyretin (TTR), to allow transport through the cerebrospinal fluid. Neurons can thus not only be provided with a sufficient T3 level via the aid of the astrocytes, as was hypothesized previously based on in situ hybridization data, but also by means of T4 deiodination by D2, directly at the blood–brain barrier level.

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

The Blood-Brain Barrier Interface in Diabetes Mellitus: Dysfunctions, Mechanisms and Approaches to Treatment

2020 ◽  
Vol 26 (13) ◽  
pp. 1438-1447 ◽  
Author(s):  
William A. Banks
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Growth Factor ◽  
Matrix Metalloproteinases ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Type I ◽  
Type Ii ◽  
P Glycoprotein ◽  
Blood Brain

Diabetes mellitus (DM) is one of the most common diseases in the world. Among its effects are an increase in the risk of cognitive impairment, including Alzheimer’s disease, and blood-brain barrier (BBB) dysfunction. DM is characterized by high blood glucose levels that are caused by either lack of insulin (Type I) or resistance to the actions of insulin (Type II). The phenotypes of these two types are dramatically different, with Type I animals being thin, with low levels of leptin as well as insulin, whereas Type II animals are often obese with high levels of both leptin and insulin. The best characterized change in BBB dysfunction is that of disruption. The brain regions that are disrupted, however, vary between Type I vs Type II DM, suggesting that factors other than hyperglycemia, perhaps hormonal factors such as leptin and insulin, play a regionally diverse role in BBB vulnerability or protection. Some BBB transporters are also altered in DM, including P-glycoprotein, lowdensity lipoprotein receptor-related protein 1, and the insulin transporter as other functions of the BBB, such as brain endothelial cell (BEC) expression of matrix metalloproteinases (MMPs) and immune cell trafficking. Pericyte loss secondary to the increased oxidative stress of processing excess glucose through the Krebs cycle is one mechanism that has shown to result in BBB disruption. Vascular endothelial growth factor (VEGF) induced by advanced glycation endproducts can increase the production of matrix metalloproteinases, which in turn affects tight junction proteins, providing another mechanism for BBB disruption as well as effects on P-glycoprotein. Through the enhanced expression of the redox-related mitochondrial transporter ABCB10, redox-sensitive transcription factor NF-E2 related factor-2 (Nrf2) inhibits BEC-monocyte adhesion. Several potential therapies, in addition to those of restoring euglycemia, can prevent some aspects of BBB dysfunction. Carbonic anhydrase inhibition decreases glucose metabolism and so reduces oxidative stress, preserving pericytes and blocking or reversing BBB disruption. Statins or N-acetylcysteine can reverse the BBB opening in some models of DM, fibroblast growth factor-21 improves BBB permeability through an Nrf2-dependent pathway, and nifedipine or VEGF improves memory in DM models. In summary, DM alters various aspects of BBB function through a number of mechanisms. A variety of treatments based on those mechanisms, as well as restoration of euglycemia, may be able to restore BBB functions., including reversal of BBB disruption.

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
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