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Am J Physiol Endocrinol Metab 285: E775-E782, 2003. First published June 24, 2003; doi:10.1152/ajpendo.00175.2003
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Effect of {beta}1- and {beta}2-adrenergic stimulation on energy expenditure, substrate oxidation, and UCP3 expression in humans

Joris Hoeks,1 Marleen A. van Baak,1 Matthijs K. C. Hesselink,2 Gabby B. Hul,1 Hubert Vidal,3 Wim H. M. Saris,1 and Patrick Schrauwen1

Departments of 1Human Biology and 2Movement Sciences, Nutrition and Toxicology Research Institute Maastricht, Maastricht University, 6200 MD Maastricht, The Netherlands; and 3Institut National de la Santé et de la Recherche Médicale Unit 449, Faculty of Medicine RTH Laennec, 69372 Lyon, France

Submitted 16 April 2003 ; accepted in final form 19 June 2003

In humans, {beta}-adrenergic stimulation increases energy and fat metabolism. In the case of {beta}1-adrenergic stimulation, it is fueled by an increased lipolysis. We examined the effect of {beta}2-adrenergic stimulation, with and without a blocker of lipolysis, on thermogenesis and substrate oxidation. Furthermore, the effect of {beta}1-and {beta}2-adrenergic stimulation on uncoupling protein 3 (UCP3) mRNA expression was studied. Nine lean males received a 3-h infusion of dobutamine (DOB, {beta}1) or salbutamol (SAL, {beta}2). Also, we combined SAL with acipimox to block lipolysis (SAL+ACI). Energy and substrate metabolism were measured continuously, blood was sampled every 30 min, and muscle biopsies were taken before and after infusion. Energy expenditure significantly increased ~13% in all conditions. Fat oxidation increased 47 ± 7% in the DOB group and 19 ± 7% in the SAL group but remained unchanged in the SAL+ACI condition. Glucose oxidation decreased 40 ± 9% upon DOB, remained unchanged during SAL, and increased 27 ± 11% upon SAL+ACI. Plasma free fatty acid (FFA) levels were increased by SAL (57 ± 11%) and DOB (47 ± 16%), whereas SAL+ACI caused about fourfold lower FFA levels compared with basal levels. No change in UCP3 was found after DOB or SAL, whereas SAL+ACI downregulated skeletal muscle UCP3 mRNA levels 38 ± 13%. In conclusion, {beta}2-adrenergic stimulation directly increased energy expenditure independently of plasma FFA levels. Furthermore, this is the first study to demonstrate a downregulation of skeletal muscle UCP3 mRNA expression after the lowering of plasma FFA concentrations in humans, despite an increase in energy expenditure upon {beta}2-adrenergic stimulation.

uncoupling protein 3; thermogenesis; adrenergic receptors; sympathetic nervous system


Address for reprint requests and other correspondence: J. Hoeks, NUTRIM, Dept. of Human Biology, Maastricht Univ., PO Box 616, 6200 MD Maastricht, The Netherlands (E-mail: j.hoeks{at}hb.unimaas.nl).




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