Ingested Ketone Ester Leads to a Rapid Rise of Acetyl-CoA and Competes with Glucose Metabolism in the Brain of Non-Fasted Mice

In non-fasted mice, oral ketone ester (3 mg per g of body weight) was given by gavage and brain metabolism was analysed by liquid chromatography with tandem mass spectrometry. Ketosis peaked at 6.83 plus or minus 0.19 mmol/L at 30 minutes after gavage. Brain beta-hydroxybutyrate uptake correlated strongly with plasma concentration and was preferentially distributed in the neocortex. Oral ketone ester increased acetyl-CoA and citric cycle intermediates in the brain, and the raised acetyl-CoA inhibited glycolysis by a feedback mechanism, competing with glucose.