title: Beta-adrenoceptor activity and resting energy metabolism in weight losing cancer patients.
abstract: This study was aimed at comparing the blocking of beta-adrenoceptor activity to changes in the resting energy metabolism of 10 cancer patients with progressive weight loss due to solid malignant tumours. Resting energy expenditure (REE) as well as whole body carbohydrate and fat oxidation were investigated and related to plasma substrate levels (glucose, glycerol, free fatty acids (FFA)) before and after 5 days of oral administration of specific beta1 receptor blocker (atenolol, 50 mg/day) and non-specific beta1,beta2-adrenoceptor (propranolol, 80 mg/day) blockade. The administration order of the drugs was random, and a 3-day washout period was used in all individuals between the provision of the first and the second drug in order to minimise the risk of carry-over effects. Resting measurements in the morning after an overnight fast were performed by indirect calorimetry. Atenolol treatment reduced REE by 77+/-14 kcal/day and propranolol by 48+/-13 kcal/day, respectively (P<0.05 versus pretreatment values). Whole body oxygen uptake and carbon dioxide production were decreased similarly by both atenolol and propranolol treatment (P<0.05). Carbohydrate oxidation was increased by atenolol and decreased by propranolol, whilst fat oxidation was decreased by atenolol and unchanged by propranolol. The decrease in REE, accounting for the decline in heart rate, was significantly more pronounced following treatment with propranolol compared with atenolol (P<0.05). Atenolol and propranolol had no effect on blood glucose, plasma glycerol and FFA. We conclude that wastage in cancer patients is in part explained by increased beta(1) and beta(2)-adrenoceptor activity, in part secondary to elevated cardiovascular activity as a result of anaemia, loss of cardiac contractile capacity and altered host metabolism.
authors.affiliation: Surgical Metabolic Research Laboratory and Lundberg Laboratory for Cancer Research, Department of Surgery, Sahlgrenska University Hospital, S-413 45, Göteborg, Sweden.
authors.forename: A
authors.initials: A
authors.lastname: Hyltander
authors.forename: P
authors.initials: P
authors.lastname: Daneryd
authors.forename: R
authors.initials: R
authors.lastname: Sandström
authors.forename: U
authors.initials: U
authors.lastname: Körner
authors.forename: K
authors.initials: K
authors.lastname: Lundholm
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D001262:Atenolol / Q000627:therapeutic use; D002100:Cachexia / Q000378:metabolism*; D002153:Calorimetry, Indirect; D050260:Carbohydrate Metabolism; D004734:Energy Metabolism / Q000187:drug effects*; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D009369:Neoplasms / Q000188:drug therapy* / Q000378:metabolism*; D011433:Propranolol / Q000627:therapeutic use; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D018709:Statistics, Nonparametric; D015431:Weight Loss
chemical_list: D000319:Adrenergic beta-Antagonists; D011943:Receptors, Adrenergic, beta; D001262:Atenolol; D011433:Propranolol