UPTAKE OF GLUCOSE ANALOGUES BY RAT BRAIN CORTEX SLICES: Na<sup>+</sup>‐INDEPENDENT MEMBRANE TRANSPORT

Lund‐Andersen, Henrik; Kjeldsen, Christel S.; Hertz, Leif; Brøndsted, H. E.

doi:10.1111/j.1471-4159.1976.tb12255.x

Cited by 17 publications

(7 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since endothelial cells (primary cell component of BBB) regulate the delivery of glucose into the brain, the BBB endothelium plays a vital role for the supply of energy and nutrients to brain cells (Lund-Andersen et al 1976). Thus, malfunctioning of the BBB is expected to adversely affect the uptake, transport, and utilization of glucose by different types of brain cells (neurons and glial cells) and their very survival.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of alcohol on glucose transport across the blood–brain barrier leads to neurodegeneration: preventive role of acetyl-l-carnitine

et al. 2010

View full text Add to dashboard Cite

Purpose-Evidence shows that alcohol intake causes oxidative neuronal injury and neurocognitive deficits that are distinct from the classical Wernicke-Korsakoff neuropathy. Our previous findings indicated that alcohol-elicited blood-brain barrier (BBB) damage leads to neuroinflammation and neuronal loss. The dynamic function of the BBB requires a constant supply and utilization of glucose. Here we examined whether interference of glucose uptake and transport at the endothelium by alcohol leads to BBB dysfunction and neuronal degeneration.Material and methods-We tested the hypothesis in cell culture of human brain endothelial cells, neurons and alcohol intake in animal by immunofluorescence, Western blotting and glucose uptake assay methods.Results-We found that decrease in glucose uptake correlates the reduction of glucose transporter protein 1 (GLUT1) in cell culture after 50 mM ethanol exposure. Decrease in GLUT1 protein levels was regulated at the translation process. In animal, chronic alcohol intake suppresses the transport of glucose into the frontal and occipital regions of the brain. This finding is validated by a marked decrease in GLUT1 protein expression in brain microvessel (the BBB). In parallel, alcohol intake impairs the BBB tight junction proteins occludin, zonula occludens-1, and claudin-5 in the brain microvessel. Permeability of sodium fluorescein and Evans Blue confirms the leakiness of the BBB. Further, depletion of trans-endothelial electrical resistance of the cell monolayer supports the disruption of BBB integrity. Administration of acetyl-L-carnitine (a neuroprotective agent) significantly prevents the adverse effects of alcohol on glucose uptake, BBB damage and neuronal degeneration.Conclusion-These findings suggest that alcohol-elicited inhibition of glucose transport at the blood-brain interface leads to BBB malfunction and neurological complications.

show abstract

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of alcohol on glucose transport across the blood–brain barrier leads to neurodegeneration: preventive role of acetyl-l-carnitine

et al. 2010

View full text Add to dashboard Cite

show abstract

“…The observation that the anoxia-resistance of RON axons was only appreciated when bath glucose concentration was three times (30 mmol/L) what is conventionally considered as normal for in vitro experiments (i.e., 10mmol/L) serves as a caution that optimal bath glucose concentration may vary from one preparation to the next. The in vitro situation imposes special demands on glucose delivery (Lund-Andersen et al, 1976). In the intact brain, delivery is via a mesh of nutritive capillaries that appear to be about 50 m apart (Bachelard et al, 1973).…”

Section: Rat Optic Nerves and Anoxiamentioning

confidence: 99%

Axon Function Persists during Anoxia in Mammalian White Matter

Tekkök

Brown

Ransom

2003

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Summary:Axon function in the CNS has been reported to fail rapidly during anoxia, implying that there is no anaerobic capacity. This phenomenon was reassessed in rodent white matter using mouse or rat optic nerve. Axon function was semiquantitatively measured as area under the compound action potential. Mouse optic nerves exposed to anoxia (30-180 minutes) or cyanide (30-60 minutes) at 37°C exhibited significant persistent function that was abolished by removing glucose. Reduction in compound action potential area increased with anoxia duration reaching a maximum of about 70% after 90 min. Rat optic nerves exposed to anoxia, in contrast to mouse optic nerves, showed rapid and complete loss of function. When artificial CSF glucose was increased from 10 to 30 mmol/L, rat optic nerves responded to anoxia in a similar manner to mouse optic nerves in 10-mmol/L glucose. The authors conclude that white matter is resistant to anoxia with a subset of axons able to subsist exclusively on anaerobically derived energy. Because the rat optic nerve is about twice the diameter of the mouse optic nerve, glucose diffusion into the rat optic nerve was inadequate during anoxia when artificial CSF glucose was 10 mmol/L but became adequate when artificial CSF glucose was 30 mmol/L. These observations have implications for white matter energy metabolism and susceptibility to injury during focal ischemia.

show abstract

“…This phenomenon was observed in guinea-pig cerebralcortex slices (Joanny et al, 1969) and in blood-brain barrier permeability studies (Oldendorf, 1971), although an accumulation of L-glucose was described in virus-transformed cell (Hatanaka, 1974). Furthermore, the characteristic Naindependence of glucose uptake in the brain (Cook et al, 1971;Pardridge and Oldendorf, 1972;Edstrom et al, 1975;and Lund-Andersen et al, 1976) was also obvious in the investigations of the cerebellar cultures.…”

Section: Discussionmentioning

confidence: 94%

Uptake of radiolabeled glucose analogues by organotypic cerebellar cultures

et al. 1978

View full text Add to dashboard Cite

Permeability of brain cells to radiolabeled glucose analogues with sucrose or inulin or L-glucose was studied in the living, intact state of the organotypic cerebellar cultures. In vitro uptake of 3H 3-O-methyl D-glucose and 3H 2-deoxy-D-glucose exhibited saturation kinetics with increasing substrate concentrations. Each of the labeled sugars uptake could be self-inhibited in the presence of unlabeled (cold) substrate and cross-inhibited with cold glucose or xylose or phlorizin present in the incubating medium. The uptake was Na-independent and stereo-specific for D-form.

show abstract

UPTAKE OF GLUCOSE ANALOGUES BY RAT BRAIN CORTEX SLICES: Na⁺‐INDEPENDENT MEMBRANE TRANSPORT

Cited by 17 publications

References 17 publications

Inhibitory effects of alcohol on glucose transport across the blood–brain barrier leads to neurodegeneration: preventive role of acetyl-l-carnitine

Inhibitory effects of alcohol on glucose transport across the blood–brain barrier leads to neurodegeneration: preventive role of acetyl-l-carnitine

Axon Function Persists during Anoxia in Mammalian White Matter

Uptake of radiolabeled glucose analogues by organotypic cerebellar cultures

Contact Info

Product

Resources

About

UPTAKE OF GLUCOSE ANALOGUES BY RAT BRAIN CORTEX SLICES: Na+‐INDEPENDENT MEMBRANE TRANSPORT

Cited by 17 publications

References 17 publications

Inhibitory effects of alcohol on glucose transport across the blood–brain barrier leads to neurodegeneration: preventive role of acetyl-l-carnitine

Inhibitory effects of alcohol on glucose transport across the blood–brain barrier leads to neurodegeneration: preventive role of acetyl-l-carnitine

Axon Function Persists during Anoxia in Mammalian White Matter

Uptake of radiolabeled glucose analogues by organotypic cerebellar cultures

Contact Info

Product

Resources

About

UPTAKE OF GLUCOSE ANALOGUES BY RAT BRAIN CORTEX SLICES: Na⁺‐INDEPENDENT MEMBRANE TRANSPORT