Inhibition of lipolysis reduces beta(1)-adrenoceptor-mediated thermogenesis in man

Citation
Slh. Schiffelers et al., Inhibition of lipolysis reduces beta(1)-adrenoceptor-mediated thermogenesis in man, METABOLISM, 47(12), 1998, pp. 1462-1467
Citations number
25
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
METABOLISM-CLINICAL AND EXPERIMENTAL
ISSN journal
00260495 → ACNP
Volume
47
Issue
12
Year of publication
1998
Pages
1462 - 1467
Database
ISI
SICI code
0026-0495(199812)47:12<1462:IOLRBT>2.0.ZU;2-3
Abstract
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.