L. Simonsen et al., GLUCOSE-INDUCED THERMOGENESIS IN PATIENTS WITH SMALL-CELL LUNG-CARCINOMA - BEFORE AND AFTER INHIBITION OF TUMOR-GROWTH BY CHEMOTHERAPY, Clinical physiology, 13(4), 1993, pp. 385-396
Seven weight-losing patients with histologically verified small cell l
ung carcinoma were given an oral glucose load of 75 g before and at le
ast 3 weeks after the end of chemotherapy to examine the effect of glu
cose on whole body and skeletal muscle thermogenesis before and after
reduction of tumour. 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 skeletal muscle was calculated as the product of the forearm blood
flow and the difference in a-v oxygen concentration. Whole body resti
ng energy expenditure (REE) did not increase, it was 4-4 +/- 0.3 kJ mi
n-1 (mean +/- SE) before chemotherapy and 4.4 +/- 0.2 kJ min-1 after c
hemotherapy. The glucose-induced thermogenesis in the 180 min followin
g the glucose load was 93.6 +/- 9.9 kJ 180 min-1 before chemotherapy.
This is significantly increased compared to that found in a healthy co
ntrol group (74.7 +/- 4.8 kJ 180 min-1, P<0.02). The glucose-induced t
hermogenesis was significantly reduced to 47.7 +/- 10.2 kJ 180 min-1 (
P<0.05) after chemotherapy. The oxygen uptake in resting skeletal musc
les was 6.9 +/- 0.3 mumol 100 g-1 min-1 before chemotherapy and 7.0 +/
- 0.7 mumol 100 g-1 min-1 after chemotherapy. This did not increase du
ring the first 90 min following the glucose load in either investigati
ons. In the period 90-180 min following the glucose load, the oxygen u
ptake was significantly increased before chemotherapy as compared to a
fter chemotherapy, which suggests that the reduced whole body thermoge
nesis after chemotherapy in part was due to reduced skeletal muscle th
ermogenesis.