Abstract
Measurements of the unidirectional blood‐brain glucose flux in rat were incompatible with a single set of kinetic constants for transendothelial transport. At least two transfer mechanisms were present: a high‐affinity, low‐capacity system, and a low‐affinity, high‐capacity system. The low‐affinity system did not represent passive diffusion because it distinguished between D‐and L‐glucose. The Tmax and Km, for the high‐affinity system were 0.16 mmol 100 g−1 min−1 and 1 mM; for the low‐affinity system, ∼ 5 mmol 100 g−1 min−1 and ∼ 1 M. With these values, physiological glucose concentrations were not sufficient to saturate the low‐affinity system. In normoglycemia, therefore, three independent pathways of glucose transport from blood to brain appear to exist: a high‐affinity facilitated diffusion pathway of apparent permeability 235·10−7 cm s−1, a specific but nonsaturable diffusion pathway of permeability 85·10−7 cm s−l, and a nonspecifc passive diffusion pathway of permeability 2·10−7 cm s−1.

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