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Abstract #3238

13C MRS During [3-13C]lactate Infusion Under Hyperinsulinemic-Hypoglycemic Conditions Reveals Compartmentalized Lactate Metabolism in Human Brain

Henk De Feyter1, Kitt Falk Petersen2, Graeme F. Mason3, Gerard Sanacora4, John Krystal4, Barbara Gulanski5, Robert S. Sherwin5, Kevin L. Behar4, Robin A. de Graaf1, Fawzi Boumezbeur6, Gerald I. Shulman2, Douglas L. Rothman1

1Diagnostic Radiology, Yale University, New Haven, CT, USA; 2Internal Medicine, Yale University, New Haven, CT, USA; 3Psychiatry, Yale University, New Haven, CT, USA; 4Department of Psychiatry, Yale University, New Haven, CT, USA; 5Department of Internal Medicine and Endocrinology, Yale University, New Haven, CT, USA; 6Neurospin, Gif-sur-Yvette, France

The brain relies on glucose as its primary energy substrate but is also able to use alternative substrates to fuel its metabolism. We present preliminary results from 13C MRS studies during [3-13C]lactate, [1-13C]glucose and [2-13C]acetate infusion to determine relative neuronal and glial consumption of blood lactate versus blood glucose. Infusion of [3-13C]lactate during hyperinsulinemic hypoglycemia to inhibit liver gluconeogenesis resulted in significant labeling of brain metabolites. In addition, simplified two-compartment metabolic modeling and comparison of the labeling patterns of brain metabolites during [1-13C]glucose and [2- 13C]acetate infusion indicate that lactate is metabolized primarily in the neuronal compartment with a similar ratio of neuronal to glial consumption as glucose.