Cerebral non-oxidative carbohydrate consumption in humans driven by adrenaline

TY - JOUR

T1 - Cerebral non-oxidative carbohydrate consumption in humans driven by adrenaline

AU - Seifert, Thomas S

AU - Brassard, Patrice

AU - Jørgensen, Thomas B

AU - Hamada, Ahmad J

AU - Rasmussen, Peter

AU - Quistorff, Bjørn

AU - Secher, Niels H

AU - Nielsen, Henning B

PY - 2009

Y1 - 2009

N2 - During brain activation, the decrease in the ratio between cerebral oxygen and carbohydrate uptake (6 O(2)/(glucose + (1)/(2) lactate); the oxygen-carbohydrate index, OCI) is attenuated by the non-selective beta-adrenergic receptor antagonist propranolol, whereas OCI remains unaffected by the beta(1)-adrenergic receptor antagonist metroprolol. These observations suggest involvement of a beta(2)-adrenergic mechanism in non-oxidative metabolism for the brain. Therefore, we evaluated the effect of adrenaline (0.08 microg kg(-1) min(-1) i.v. for 15 min) and noradrenaline (0.5, 0.1 and 0.15 microg kg(-1) min(-1) i.v. for 20 min) on the arterial to internal jugular venous concentration differences (a-v diff) of O(2), glucose and lactate in healthy humans. Adrenaline (n = 10) increased the arterial concentrations of O(2), 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 beta(2)-adrenergic mechanism, giving neurons an abundant provision of energy when plasma adrenaline increases Udgivelsesdato: 2009/1/15

AB - During brain activation, the decrease in the ratio between cerebral oxygen and carbohydrate uptake (6 O(2)/(glucose + (1)/(2) lactate); the oxygen-carbohydrate index, OCI) is attenuated by the non-selective beta-adrenergic receptor antagonist propranolol, whereas OCI remains unaffected by the beta(1)-adrenergic receptor antagonist metroprolol. These observations suggest involvement of a beta(2)-adrenergic mechanism in non-oxidative metabolism for the brain. Therefore, we evaluated the effect of adrenaline (0.08 microg kg(-1) min(-1) i.v. for 15 min) and noradrenaline (0.5, 0.1 and 0.15 microg kg(-1) min(-1) i.v. for 20 min) on the arterial to internal jugular venous concentration differences (a-v diff) of O(2), glucose and lactate in healthy humans. Adrenaline (n = 10) increased the arterial concentrations of O(2), 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 beta(2)-adrenergic mechanism, giving neurons an abundant provision of energy when plasma adrenaline increases Udgivelsesdato: 2009/1/15

U2 - 10.1113/jphysiol.2008.162073

DO - 10.1113/jphysiol.2008.162073

M3 - Journal article

C2 - 19015195

SN - 0022-3751

VL - 587

SP - 285

EP - 293

JO - The Journal of Physiology

JF - The Journal of Physiology

IS - Pt 1

ER -