Effect of β-Adrenergic Blockade on Resting and Stimulated Fat Mobilization

Abstract

Some metabolic effects of an acute β-adrenergic receptor blockade were studied in 34 healthy subjects. Plasma free fatty acid (FFA) and blood glucose levels were determined in all, and kinetic data of plasma FFA were obtained in several of these individuals. β-Adrenergic receptor blockade was induced by intravenous propranolol [l-isopropylamino-3-(l-naphthyloxy)-2-propanol hydrochloride] infusion (0.3 mg/kg/15 min). The influence of propranolol on fat mobilization was studied at metabolic rest and during both exogenous (adrenergic) and endogenous (mixed) stimulation of adipokinesis (intravenous infusion of 0.5 μg/kg/15 min of epinephrine and starvation >55 hr, respectively). At metabolic rest propranolol caused a slight drop in plasma FFA levels, due to a transient decrease in FFA production rate and an equally nonsignificant rise in the blood glucose concentrations. The adipokinetic effectiveness of the intravenous epinephrine infusion, on the other hand, was markedly suppressed by the prior administration of propranolol, due to a primary effect of β-adrenergic receptor blockade on FFA production rate (82.7% inhibition of the epinephrine-induced rise). The hyperglycemic effect of epinephrine remained unaffected. β-Adrenergic receptor blockade induced during prolonged starvation failed to alter markedly and/or uniformly the concentration and the kinetic behavior of plasma FFA. No significant changes were shown in the blood glucose concentrations of the slightly hypoglycemic starving subjects. No indication of an intrinsic (fat mobilizing) activity of propranolol was found. The evidence obtained in this study is compatible with the primary role of β-receptors in hyperadipokinesis initiated by an adrenergic mechanism. The contribution of the endogenous catecholamines to the maintenance of the resting rate of fat mobilization and to the hyperadipokinesis of starvation is, on the other hand, slight or at least secondary. It is proposed that the β-adrenergic receptors in the adipose tissue cannot be considered as hypothetical “ultimate receptors” for the mediation of the lipolytic action of the diverse adipokinetic hormones.