BLOOD-BRAIN GLUCOSE TRANSFER IN THE MOUSE

The intracarotid injection method has been utilized to examine blood-b rain barrier (BBB) glucose transport in normal mice, and after a 2-day fast. In anesthetized mice, cerebral blood flow (CBF) rates were redu ced from 0.86 ml.min-1.gm-1 in control to 0.80 ml.min-1.gm-1 in fasted animals (p > 0.05). Brain Uptake Indices were significantly (p < 0.05 ) higher in fasted (plasma glucose = 4.7 mM) than control (plasma gluc ose = 6.5 mM) mice, while plasma glucose was significantly lower. The maximal velocity (V(max)) for glucose transport was 1562 +/- 303 nmole s.min-1.g-1, and the half-saturation constant (Km =) 6.67 +/- 1.46 mM in normally fed mice. In fasted mice the Vmax was 2053 +/- 393 nmoles. min-1.g-1 (p > 0.05), and the half-saturation constant (Km =) 7.40 +/- 1.60 mM (not significant, P > 0.05). A rabbit polyclonal antiserum to a synthetic peptide encoding the 13 C-terminal amino acids of the hum an erythrocyte glucose transporter (GLUT-1) immunocytochemically confi rmed that the mouse brain capillary endothelial glucose transporter is a GLUT-1 transporter, and immunoreactivity was similar in brain endot helia from fed and fasted animals. In conclusion, after a 2-day fast i n the mouse, we saw significant reductions in forebrain weight (7%), a nd plasma glucose levels (27%). Increased brain glucose extraction (25 %, p < 0.05), and a 22% increase in the unsaturated permeability-surfa ce area product (p < 0,05) was also observed.