Inhibition of lipolysis reduces beta1-adrenoceptor-mediated thermogenesis in man.

The purpose of the study was to investigate whether the increase in energy expenditure and lipid oxidation during beta1-adrenergic stimulation is caused by the concomitant increase in lipolysis. Twelve healthy male subjects participated in three trials: no-LIP/-, inhibition of lipolysis by pretreatment with acipimox followed by saline infusion; -/BETA, no pretreatment, with dobutamine infusion to stimulate beta1-adrenoceptors; and no-LIP/BETA, pretreatment with acipimox followed by dobutamine infusion. Inhibition of lipolysis did not affect baseline energy expenditure, but decreased lipid oxidation and increased carbohydrate oxidation. Energy expenditure and lipid oxidation increased significantly during beta1-adrenergic stimulation, but this increase was significantly smaller when lipolysis was inhibited ([baseline v infusion period] energy expenditure: -/BETA, 5.15 +/- 0.16 v 6.11 +/- 0.26 kJ/min, P < .001; no-LIP/BETA, 5.28 +/- 0.17 v 5.71 +/- 0.19 kJ/min, P < .01; lipid oxidation: -/BETA, 0.059 +/- 0.004 v 0.073 +/- 0.006 g/min, P < .01; no-LIP/BETA, 0.034 +/- 0.005 v 0.039 +/- 0.006 g/min, P < .05). Baseline plasma glycerol and nonesterified fatty acid (NEFA) concentrations decreased after inhibition of lipolysis. Glycerol and NEFA increased significantly during beta1-adrenergic stimulation alone (glycerol, 65.0 +/- 5.3 v 117.0 +/- 10.9 micromol/L; NEFA, 362 +/- 24 v 954 /- 89 micromol/L; both P < .001). Concomitant administration of acipimox prevented a substantial part of the increase in lipolysis during beta1-adrenergic stimulation, but the increase in plasma glycerol and NEFA remained significant (glycerol, 40.4 +/- 2.2 v 44.8 +/- 2.2 micromol/L; NEFA, 118 +/- 18 v 160 +/- 19 micromol/L; both P < .05). In conclusion, a reduced availability of plasma NEFA was associated with a reduced increase in energy expenditure and lipid oxidation during beta1-adrenergic stimulation in man.