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

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 beta-adrenoceptor-mediated responses in lipid utilization and t...

Full description

Saved in:
Bibliographic Details
Published in:American journal of physiology: endocrinology and metabolism 2001-02, Vol.280 (2), p.E357-E364
Main Authors: Schiffelers, S L, Blaak, E E, Baarends, E M, Van Baak, M A, Saris, W H, Wouters, E F, Schols, A M
Format: Article
Language:English
Subjects:
Adrenergic beta-Agonists - blood
Adrenergic beta-Agonists - pharmacology
Body Temperature Regulation - physiology
Energy Metabolism
Fatty Acids, Nonesterified - blood
Heart Rate - drug effects
Humans
Isoproterenol - blood
Isoproterenol - pharmacology
Lipolysis - physiology
Lung Diseases, Obstructive - physiopathology
Male
Middle Aged
Norepinephrine - blood
Pulmonary Gas Exchange - drug effects
Receptors, Adrenergic, beta - physiology
Reference Values
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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 beta-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 x kg fat free mass(-1) x min(-1) isoproterenol. During beta-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 beta-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, beta-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.
ISSN:0193-1849
1522-1555
DOI:10.1152/ajpendo.2001.280.2.e357