Blood-brain glucose transfer in the mouse.

The intracarotid injection method has been utilized to examine blood-brain barrier (BBB) glucose transport in normal mice, and after a 2-day fast. In anesthetized mice, cerebral blood flow (CBF) rates were reduced from 0.86 ml.min-1 x gm-1 in control to 0.80 ml.min-1 x 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 glucose = 6.5 mM) mice, while plasma glucose was significantly lower. The maximal velocity (Vmax) for glucose transport was 1562 +/- 303 nmoles.min-1 x 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 x 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 human erythrocyte glucose transporter (GLUT-1) immunocytochemically confirmed that the mouse brain capillary endothelial glucose transporter is a GLUT-1 transporter, and immunoreactivity was similar in brain endothelia from fed and fasted animals. In conclusion, after a 2-day fast in the mouse, we saw significant reductions in forebrain weight (7%), and plasma glucose levels (27%). Increased brain glucose extraction (25%, p < 0.05), and a 22% increase in the unsaturated permeability-surface area product (p < 0.05) was also observed.