Glucose-induced thermogenesis in patients with small cell lung carcinoma. The effect of acute beta-adrenergic inhibition.

Abstract

Seven patients with histologically verified small cell lung carcinoma were given an oral glucose load of 75 g on two occasions to examine the effect of glucose on whole body and forearm thermogenesis with and without acute beta-adrenergic inhibition with propranolol. Whole body energy expenditure was measured by the open circuit ventilated hood system. Forearm blood flow was measured by venous occlusion strain-gauge plethysmography. The uptake of oxygen in the forearm was calculated as the product of the forearm blood flow and the difference in arteriovenous oxygen concentration. The glucose-induced thermogenesis in the 120 min following the glucose load was significantly reduced by beta-adrenergic inhibition with approximately 50% from 63.9 +/- 5.8 kJ 120 min-1 (mean +/- SE) to 27.8 +/- 9.8 kJ 120 min-1 (P < 0.01). Almost the entire reduction took place from 60 to 120 min (P < 0.005). The integrated glucose-induced forearm oxygen uptake in the period 60-120 min following the glucose load was significantly reduced after beta-adrenergic inhibition from 103 +/- 28 mumol 100 g-1 60 min-1 to 29 +/- 29 mumol 100 g-1 60 min-1 (P < 0.05). The noreadrenaline concentration in the arterial blood was not increased in the baseline period compared to healthy elderly; it increased following the glucose load while there was no demonstrable increase in adrenaline concentration in the two experiments. It is suggested that these patients have increased sensitivity of the beta-adrenergic receptors and an early facultative component of the glucose-induced thermogenesis in part takes place in the forearm.