Journal
AMERICAN JOURNAL OF CLINICAL NUTRITION
Volume 76, Issue 4, Pages 780-788Publisher
ELSEVIER SCIENCE INC
DOI: 10.1093/ajcn/76.4.780
Keywords
L-796568; beta(3)-adrenergic receptor; beta(3)-adrenergic receptor agonist; beta(3) agonist; selectivity; energy expenditure; lipolysis; respiratory quotient; indirect calorimetry; triacylglycerol; obesity; obese men
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Background: Stimulation of energy expenditure (EE) with selective thermogenic P-adrenergic agonists may be a promising approach for treating obesity. Objective: We analyzed the effects of the highly selective human beta(3)-adrenergic agonist L-796568 on 24-h EE, substrate oxidation, and body composition in obese, weight-stable men. Design: In this 2-center, double-blind, randomized, parallel-group study, we measured 24-h EE before and after 28 d of treatment with L-796568 (375 mg/d) or placebo during weight maintenance (ie, without dietary intervention) in nondiabetic, nonsmoking men aged 25-49 y with body mass index (in kg/m(2)) of 28-35 (n = 10 subjects per treatment group). Results: The mean change in 24-h EE from before to after treatment did not differ significantly between groups (92 586 and 86 512 kJ/24 h for the L-796568 and placebo groups, respectively). The change in 24-h nonprotein respiratory quotient from before to after treatment did not differ significantly between groups (0.009 +/- 0.021 and 0.009 +/- 0.029, respectively). No changes in glucose tolerance were observed, but triacylglycerol concentrations decreased significantly with L-796568 treatment compared with placebo (-0.76 +/- 0.76 and 0.42 +/- 0.31 mmol/L, respectively; P < 0.002). Overall, treatment-related changes in body composition were not observed, but higher plasma L-796568 concentrations in the L-796568 group were associated with greater decreases in fat mass (r = -0.69, P < 0.03). Conclusions: Treatment with L-796568 for 28 d had no major lipolytic or thermogenic effect but it lowered triacylglycerol concentrations. This lack of chronic effect on energy balance is likely explained by insufficient recruitment of beta(3)-responsive tissues in humans, down-regulation of the beta(3)-adrenergic receptormediated effects with chronic dosing, or both.
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