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

The present study investigated whether development or maintenance of a rela tively increased fat mass in normal-weight patients with chronic obstructiv e pulmonary disease (COPD), despite periods of weight loss, may be related to impaired beta -adrenoceptor-mediated responses in lipid utilization and thermogenesis. Nine COPD patients and nine healthy controls (body mass inde x: 23.0 +/- 1.3 vs. 23.8 +/- 0.6 kg/m(2), 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 <be ta>-adrenergic stimulation, nonesterified fatty acid levels increased signi ficantly less in COPD patients (P < 0.001). Respiratory exchange ratio decr eased similarly in both groups, indicating a similar change in the rate of lipid to carbohydrate oxidation. Energy expenditure increased similarly in both groups during <beta>-adrenergic stimulation. However, because plasma i soproterenol concentrations were significantly higher in COPD patients, the rmogenesis related to isoproterenol concentration was significantly reduced in this group (P < 0.05). In conclusion, <beta>-adrenoceptor-mediated lipo lysis and thermogenesis are impaired in COPD patients. This may play a role in the development or maintenance of their relatively increased fat mass.