Molecular and Cellular Biochemistry

, Volume 140, Issue 2, pp 177–184

Glucose transport in developing rat brain: Glucose transporter proteins, rate constants and cerebral glucose utilization

Authors

  • Susan J. Vannucci
    • Department of Pediatrics (Pediatric Neurology)The Pennsylvania State University School of Medicine, The Milton S. Hershey Medical Center
  • Lisa B. Seaman
    • Department of Pediatrics (Pediatric Neurology)The Pennsylvania State University School of Medicine, The Milton S. Hershey Medical Center
  • Robert M. Brucklacher
    • Department of Pediatrics (Pediatric Neurology)The Pennsylvania State University School of Medicine, The Milton S. Hershey Medical Center
  • Robert C. Vannucci
    • Department of Pediatrics (Pediatric Neurology)The Pennsylvania State University School of Medicine, The Milton S. Hershey Medical Center
Article

DOI: 10.1007/BF00926756

Cite this article as:
Vannucci, S.J., Seaman, L.B., Brucklacher, R.M. et al. Mol Cell Biochem (1994) 140: 177. doi:10.1007/BF00926756

Abstract

Developing rat brain undergoes a series of functional and anatomic changes which affect its rate of cerebral glucose utilization (CGU). These changes include increases in the levels of the glucose transporter proteins, GLUT1 and GLUT3, in the blood-brain barrier as well as in the neurons and glia. 55 kDa GLUT1 is concentrated in endothelial cells of the blood-brain barrier, whereas GLUT3 is the predominant neuronal transporter. 45 kDa GLUT1 is in non-vascular brain, probably glia. Studies of glucose utilization with the 2-14C-deoxyglucose method of Sokoloffet al., (1977), rely on glucose transport rate constants, k1 and k2, which have been determined in the adult rat brain. The determination of these constants directly in immature brain, in association with the measurement of GLUT1, GLUT3 and cerebral glucose utilization suggests that the observed increases in the rate constants for the transport of glucose into (k1) and out of (k2) brain correspond to the increases in 55 kDa GLUT1 in the blood-brain barrier. The maturational increases in cerebral glucose utilization, however, more closely relate to the pattern of expression of non-vascular GLUT1 (45 kDa), and more specifically GLUT3, suggesting that the cellular expression of the glucose transporter proteins is rate limiting for cerebral glucose utilization during early postnatal development in the rat.

Key words

GLUT1 proteinGLUT3 proteinglucose transportcerebral glucose utilizationbraindevelopment

Copyright information

© Kluwer Academic Publishers 1994