This investigation was supported in part by Grant NB 06163 and the Allen P. and Josephine B. Green Foundation.
PERMEABILITY OF THE BLOOD-BRAIN BARRIER TO FRUCTOSE AND THE ANAEROBIC USE OF FRUCTOSE IN THE BRAINS OF YOUNG MICE1
Version of Record online: 4 OCT 2006
Journal of Neurochemistry
Volume 19, Issue 7, pages 1685–1696, July 1972
How to Cite
Thurston, J. H., Levy, C. A., Warren, S. K. and Jones, E. M. (1972), PERMEABILITY OF THE BLOOD-BRAIN BARRIER TO FRUCTOSE AND THE ANAEROBIC USE OF FRUCTOSE IN THE BRAINS OF YOUNG MICE. Journal of Neurochemistry, 19: 1685–1696. doi: 10.1111/j.1471-4159.1972.tb06213.x
- Issue online: 4 OCT 2006
- Version of Record online: 4 OCT 2006
- Received 1 February 1972. Accepted 3 March 1972
—Fructose levels were determined in plasma and brain of 8- to 12-day-old mice at intervals after the injection of 30 mmol/kg intraperitoneally; controls received NaCl, 15 mmol/kg. In normal animals brain fructose increased very slowly despite a rapid rise in plasma levels (120 times the control value in 5 min). At 40 min the cerebral level was 1.54 ± 0.23 mmol/kg; the corresponding plasma level was 47.1 ± 4.8 mM. The data suggest that fructose can serve as a source of energy to the brain in times of critical need: during insulin hypoglycemia brain fructose increased to only 0.88 ± 0.05 mmol/kg during the same interval (40 min) despite plasma fructose values equal to those in control animals; also 30 s after cerebral ischemia (decapitation) brain fructose fell from a zero time value of 1.19 ± 0.09 mmol/kg (20 min after fructose injection) to 0.76 ± 0.06 mmol/kg (P= 0.005). Under both circumstances (hypoglycemia and ischemie anoxia) an apparent threshold concentration of fructose for utilization was observed—0.6–0.7 mmol/kg. The most likely explanation for this finding appears to be that this level of fructose was in the extracellular space of the brain. Hexokinase activity in brain homogenates of 8- to 12-day-old mice with fructose and ATP at concentrations found in vivo and during ischemie anoxia did not appear to be rate-limiting. We concluded that the major handicap to the use of fructose by the brain was the limited penetration of fructose from the blood to the brain.