The purpose of the study was to investigate whether the increase in energy
expenditure and lipid oxidation during beta(1)-adrenergic stimulation is ca
used by the concomitant increase in lipolysis. Twelve healthy male subjects
participated in three trials: no-LIP/-, inhibition of lipolysis by pretrea
tment with acipimox followed by saline infusion; -/BETA, no pretreatment, w
ith dobutamine infusion to stimulate beta(1)-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 lipi
d oxidation increased significantly during beta(1)-adrenergic stimulation,
but this increase was significantly smaller when lipolysis was inhibited ([
baseline v infusion period] energy expenditure: -/BETA, 5.15 +/- 0.16 v 6.1
1 +/- 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) concentrati
ons decreased after inhibition of lipolysis. Glycerol and NEFA increased si
gnificantly during beta(1)-adrenergic stimulation alone (glycerol, 65.0 +/-
5.3 v 117.0 +/- 10.9 mu mol/L; NEFA, 362 +/- 24 v 954 +/- 89 mu mol/L; bot
h P < .001). Concomitant administration of acipimox prevented a substantial
part of the increase in lipolysis during beta(1)-adrenergic stimulation, b
ut the increase in plasma glycerol and NEFA remained significant (glycerol,
40.4 +/- 2.2 v 44.8 +/- 2.2 mu mol/L; NEFA, 118 +/- 18 v 160 +/- 19 mu mol
/L; both P < .05). In conclusion, a reduced availability of plasma NEFA was
associated with a reduced increase in energy expenditure and lipid oxidati
on during beta(1)-adrenergic stimulation in man. Copyright (C) 1998 by W.B.
Saunders Company.