Glucose transporters and glucose utilization in rat brain after acute ethanol administration

In the normal adult brain, glucose provides 90% of the energy requirements as well as substrate for nucleic acid and lipid synthesis. In the present study, effects of ethanol on glucose transporters (GLUT) and glucose utilization were examined in rat brain. Male Sprague-Dawley rats weighing 250-300 gms were given either ethanol 3 gm/kg BW or saline i.p. 4 hrs prior to the animal sacrifice and removal of the cerebral cortical tissue. The cortical plasma membranes analyzed by cytochalasin B binding assay showed a decrease in GLUT number but not in GLUT affinity in the ethanol treated rats as compared to the control rats. The estimated Ro values were 70 +/- 8.9 Vs 91 +/- 8.9 pmoles/mg protein (p < 0.05 N=4) and the estimated Kd values were 0.37 +/- 0.03 and 0.28 +/- 0.05 microM (p: NS) in ethanol and control experiments respectively. Immunoblots of purified cerebral plasma membranes and low density microsomal fraction showed 17% and 71% decrease for GLUTI and 54% and 21% (p<0.05 or less; n=6) for GLUT3 respectively in ethanol treated rats than in control animals. Immunofluoresence studies also showed reduction of GLUT1 immunoreactively in choroid plexus and cortical microvessels of ethanol treated rats as compared to control rats. The effect of ethanol on regional cerebral metabolic rates for glucose (CMR(Glc)) was studied using [6-(14)C] glucose and showed statistically insignificant decrease in brain glucose utilization. These data suggest that ethanol in-vivo decrease GLUT number and protein content in rat cerebral cortex.