Cerebral non-oxidative carbohydrate consumption in humans driven by adrenaline

Abstract

During brain activation, the decrease in the ratio between cerebral oxygen and carbohydrate uptake (6 O₂/(glucose + ¹/₂ lactate); the oxygen–carbohydrate index, OCI) is attenuated by the non-selective β-adrenergic receptor antagonist propranolol, whereas OCI remains unaffected by the β₁-adrenergic receptor antagonist metroprolol. These observations suggest involvement of a β₂-adrenergic mechanism in non-oxidative metabolism for the brain. Therefore, we evaluated the effect of adrenaline (0.08 μg kg⁻¹ min⁻¹i.v. for 15 min) and noradrenaline (0.5, 0.1 and 0.15 μg kg⁻¹ min⁻¹i.v. for 20 min) on the arterial to internal jugular venous concentration differences (a-v diff) of O₂, glucose and lactate in healthy humans. Adrenaline (n = 10) increased the arterial concentrations of O₂, glucose and lactate (P < 0.05) and also increased the a-v diff for glucose from 0.6 ± 0.1 to 0.8 ± 0.2 mm (mean ± s.d.; P < 0.05). The a-v diff for lactate shifted from a net cerebral release to an uptake and OCI was lowered from 5.1 ± 1.5 to 3.6 ± 0.4 (P < 0.05) indicating an 8-fold increase in the rate of non-oxidative carbohydrate uptake during adrenaline infusion (P < 0.01). Conversely, noradrenaline (n = 8) did not affect the OCI despite an increase in the a-v diff for glucose (P < 0.05). These results support that non-oxidative carbohydrate consumption for the brain is driven by a β₂-adrenergic mechanism, giving neurons an abundant provision of energy when plasma adrenaline increases.