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ß₂-Adrenergic Receptor Polymorphisms and Salbutamol-Stimulated Energy Expenditure

Department of Human Biology/NUTRIM (J.M.O., W.H.M.S., M.A.v.B.), Maastricht University, 6200 MD Maastricht, The Netherlands; and Department of Chronic Diseases Epidemiology (C.T.M.v.R.) and Laboratory of Health Effects Research (B.H.), National Institute of Public Health and the Environment, 3720 BA Bilthoven, The Netherlands

Address all correspondence and requests for reprints to: J. M. Oomen, Department of Human Biology, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands. E-mail: j.oomen{at}hb.unimaas.nl.

The ß-adrenergic system is involved in the control of energy metabolism and expenditure. The ß₂-adrenergic receptor (ß₂-AR) gene shows polymorphisms that have been associated with obesity in several studies. In vitro and in vivo studies suggest differences in ß₂-AR-mediated function between these polymorphisms. The aim of this study was to investigate the influence of genetic variation in codon 16 of the ß₂-AR gene on energy metabolism in humans.

Thirty-four subjects were recruited [Gly16Gly (n = 13), Gly16Arg (n = 16), or Arg16Arg (n = 5)]. The ß₂-AR was stimulated with two doses of salbutamol (50 and 100 ng/kg fat-free mass per minute) after blockade of the ß₁-adrenergic receptors with atenolol. Energy expenditure and plasma substrate and hormone concentrations were measured.

The increase in energy expenditure (EE) was significantly different among groups in which the Arg16Arg group showed the lowest increase (P < 0.05 vs. Gly carriers). In a multiple regression model, variations in the increase in nonesterified fatty acid concentration during salbutamol infusion (partial r = 0.51) and the polymorphism contributed significantly to the variation in EE. Thirty-five percent of the variation in EE was explained by these two factors.

We conclude that subjects with the Arg16Arg polymorphism of the ß₂-AR gene have a reduced thermogenic response to ß₂-adrenergic stimulation. Although this relatively small study needs confirmation, the findings support a role for this polymorphism in the development and maintenance of overweight and obesity.

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