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 + 1/2lactate); OCI] is attenuated by the non‐selective beta‐adrenergic receptor antagonist propranolol, whereas OCI remains unaffected by the beta1‐adrenergic receptor antagonist metroprolol. These observations suggest involvement of a beta2‐adrenergic mechanism in non‐oxidative metabolism for the brain. Therefore, we evaluated the effect of adrenaline (0.08 micrograms kg‐1 min‐1 iv. for 15 min) and noradrenaline (0.5, 0.1 and 0.15 micrograms kg‐1 min‐1 iv. 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 ± SD; 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 a 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 beta2‐adrenergic mechanism, making neurons abundantly provided with energy when plasma adrenaline increases.