β-Adrenoceptor-mediated thermogenesis and lipolysis in patients with chronic obstructive pulmonary disease

Abstract

The present study investigated whether development or maintenance of a relatively increased fat mass in normal-weight patients with chronic obstructive pulmonary disease (COPD), despite periods of weight loss, may be related to impaired β-adrenoceptor-mediated responses in lipid utilization and thermogenesis. Nine COPD patients and nine healthy controls (body mass index: 23.0 ± 1.3 vs. 23.8 ± 0.6 kg/m2, not significant; fat mass: 19.0 ± 2.1 vs. 11.9 ± 1.5 kg, P < 0.01) received consecutive 30-min infusions of 6, 12, and 24 ng · kg fat free mass−1 · min−1 isoproterenol. During β-adrenergic stimulation, nonesterified fatty acid levels increased significantly less in COPD patients ( P < 0.001). Respiratory exchange ratio decreased similarly in both groups, indicating a similar change in the rate of lipid to carbohydrate oxidation. Energy expenditure increased similarly in both groups during β-adrenergic stimulation. However, because plasma isoproterenol concentrations were significantly higher in COPD patients, thermogenesis related to isoproterenol concentration was significantly reduced in this group ( P < 0.05). In conclusion, β-adrenoceptor-mediated lipolysis and thermogenesis are impaired in COPD patients. This may play a role in the development or maintenance of their relatively increased fat mass.