Glucose transporters in the cms

Development, injury and disease

S. J. Vannucci, Ian Simpson

Research output: Contribution to journalArticle

Abstract

Glucose is the primary metabolic fuel for the mammalian brain and a continuous supply of this nutrient is essential to maintain normal cerebral function. The passage of glucose from the blood to the brain is mediated by the facultative glucose transporter proteins (GLUTs). SS kDa GLUT1 is in the endothelial cells of the blood-brain barrier (BBB), 45 kDa GLUT1 exists throughout the parenchyma, GLUTS is neuronal, and GLUTS is expressed by microglia. Levels of GLUTs 1 & 3 are low in the immature brain, consistent with low rates of cerebral glucose utilization (CGU), and increase with cerebral maturation. In Alzheimer's disease, regional decreases in GLUTs 1 & 3 coincide with deficits in CGU. The expression of both transporters is acutely increased in response to cerebral metabolic stress, such as in hypoxiaischemia, in immature and adult brains; GLUTS increases dramatically with the microglial response to injury. Thus, the le vels of all of the GLUTs appear to be closely related to the functional state and metabolic demands of the brain, and contribute to alterations in CGU observed in conditions such as hyper- and hypoglycémie, seizures and stroke.

Original languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number3
StatePublished - 1996

Fingerprint

glucose transporters
Facilitative Glucose Transport Proteins
Brain
brain
glucose
Wounds and Injuries
Glucose
immatures
Physiological Stress
blood-brain barrier
Endothelial cells
neuroglia
Microglia
Alzheimer disease
seizures
Blood-Brain Barrier
stroke
Nutrients
endothelial cells
transporters

All Science Journal Classification (ASJC) codes

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

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Glucose transporters in the cms : Development, injury and disease. / Vannucci, S. J.; Simpson, Ian.

In: FASEB Journal, Vol. 10, No. 3, 1996.

Research output: Contribution to journalArticle

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