RT Journal Article SR Electronic T1 Brain Glucose Transport and Phosphorylation Under Acute Insulin-Induced Hypoglycemia in Mice: An 18F-FDG PET Study JF Journal of Nuclear Medicine JO J Nucl Med FD Society of Nuclear Medicine SP 2153 OP 2160 DO 10.2967/jnumed.113.122812 VO 54 IS 12 A1 Malte F. Alf A1 João M.N. Duarte A1 Roger Schibli A1 Rolf Gruetter A1 Stefanie D. Krämer YR 2013 UL http://jnm.snmjournals.org/content/54/12/2153.abstract AB We addressed the questions of how cerebral glucose transport and phosphorylation change under acute hypoglycemia and what the underlying mechanisms of adaptation are. Methods: Quantitative 18F-FDG PET combined with the acquisition of real-time arterial input function was performed on mice. Hypoglycemia was induced and maintained by insulin infusion. PET data were analyzed with the 2-tissue-compartment model for 18F-FDG, and the results were evaluated with Michaelis–Menten saturation kinetics. Results: Glucose clearance from plasma to brain (K1,glc) and the phosphorylation rate constant increased with decreasing plasma glucose (Gp), in particular at a Gp of less than 2.5 mmol/L. Estimated cerebral glucose extraction ratios taking into account an increased cerebral blood flow (CBF) at a Gp of less than 2 mmol/L were between 0.14 and 0.79. CBF-normalized K1,glc values were in agreement with saturation kinetics. Phosphorylation rate constants indicated intracellular glucose depletion at a Gp of less than 2–3 mmol/L. When brain regions were compared, glucose transport under hypoglycemia was lowest in the hypothalamus. Conclusion: Alterations in glucose transport and phosphorylation, as well as intracellular glucose depletion, under acute hypoglycemia can be modeled by saturation kinetics taking into account an increase in CBF. Distinct transport kinetics in the hypothalamus may be involved in its glucose-sensing function.