We have previously shown that the increase in energy expenditure following glucose/insulin infusion is, in large part, mediated by the sympathetic nervous system and that this sympathetic component can be blocked by the nonselective beta-1, beta-2 antagonist propranolol. To examine which beta adrenergic receptor mediates this thermogenic response, we performed euglycemic insulin clamp studies in eight healthy control subjects with and without metoprolol at a dose known to block only the beta-1 adrenergic receptor. Basal glucose oxidation and energy expenditure were similar in the control and metoprolol groups. During the last hour of the insulin clamp study, glucose oxidation (3.06 ± 0.25 v 2.92 ± 0.21 mg/kg · min), total body glucose uptake (8.17 ± 0.70 v 7.13 ± 0.49 mg/kg · min), and nonoxidative glucose uptake (5.11 ± 0.60 v 4.21 ± 0.44 mg/kg · min) were not different in the control compared to the metoprolol group. However, the increment in energy expenditure was inhibited by 64% during metoprolol infusion (0.04 ± 0.01 v 0.11 ± 0.02 kcal/min, P < 0.01). Glucose/insulin-induced thermogenesis was similarly reduced by metoprolol (2.56 ± 0.81 v 5.04 ± 0.74%, P < 0.01). These results are quantitatively quite similar to those observed with propranolol. We conclude that the beta adrenergic nervous system and, specifically, the beta-1 receptor mediates the thermogenic response to glucose/insulin infusion.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism