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Blood-Brain Barrier Transport and Brain Metabolism of Glucose during Acute Hyperglycemia in Humans¹

Neurobiology Research Unit, Department of Neurology, and the PET and Cyclotron Unit, University Hospital, Rigshospitalet (S.G.H., G.M.K., O.B.P.), DK-2100 Copenhagen, Denmark; and Institute of Internal Medicine and Metabolic Diseases, Universita Degli Studi Di Napoli Federico II (B.C., A.P.), 80131 Naples, Italy

Address all correspondence and requests for reprints to: Steen G. Hasselbalch, M.D., Neurobiology Research Unit, Building 9201, National University Hospital, Rigshospitalet, 9 Blegdamsvej, DK-2100 Copenhagen Ø, Denmark. E-mail: sgh{at}pet.rh.dk

It is controversial whether transport adaptation takes place in chronic or acute hyperglycemia. Blood-brain barrier glucose permeability and regional brain glucose metabolism (CMR_glc) was studied in acute hyperglycemia in six normal human subjects (mean age, 23 yr) using the double indicator method and positron emission tomography and [¹⁸F]fluorodeoxyglucose as tracer. The Kety-Schmidt technique was used for measurement of cerebral blood flow (CBF). After 2 h of hyperglycemia (15.7 ± 0.7 mmol/L), the glucose permeability-surface area product from blood to brain remained unchanged (0.050 ± 0.008 vs. 0.059 ± 0.031 mL/100 g·min). The unidirectional clearance of [¹⁸F]fluorodeoxyglucose (K₁*) was reduced from 0.108 ± 0.011 to 0.061 ± 0.005 mL/100 g·min (P < 0.0004). During hyperglycemia, global CMR_glc remained constant (21.4 ± 1.2 vs. 23.1 ± 2.2 µmol/100 g·min, normo- and hyperglycemia, respectively). Except for a significant increase in white matter CMR_glc, no regional difference in CMR_glc was found. Likewise, CBF remained unchanged.

The reduction in K₁* was compatible with Michaelis-Menten kinetics for facilitated transport. Our findings indicate no major adaptational changes in the maximal transport velocity or affinity to the blood-brain barrier glucose transporter. Finally, hyperglycemia did not change global CBF or CMR_glc.

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