Defective Glucose Transport across the Blood-Brain Barrier as a Cause of Persistent Hypoglycorrhachia, Seizures, and Developmental Delay

  • De Vivo D
  • Trifiletti R
  • Jacobson R
  • et al.
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Abstract

GLUCOSE (D-glucose) is an essential fuel for the brain and many other tissues. Five glucose-transporter proteins facilitate the diffusion of glucose across lipophilic plasma membranes.1 2 3 This process is saturable and stereospecific, but it is not concentrative, energy dependent, or influenced by sodium. In humans, the erythrocyte glucose transporter (type 1 glucose transporter) has been studied most extensively. It accounts for 2 to 5 percent of the erythrocyte-membrane protein and seems to be identical in molecular weight and antigenic properties to the glucose transporters in the endothelial cells of brain capillaries.4 5 6 7 Brain capillaries contain large amounts of messenger RNA for the . . .

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De Vivo, D. C., Trifiletti, R. R., Jacobson, R. I., Ronen, G. M., Behmand, R. A., & Harik, S. I. (1991). Defective Glucose Transport across the Blood-Brain Barrier as a Cause of Persistent Hypoglycorrhachia, Seizures, and Developmental Delay. New England Journal of Medicine, 325(10), 703–709. https://doi.org/10.1056/nejm199109053251006

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