METABOLIC CHANGES IN ELDERLY CANCER-PATIENTS AFTER GLUCOSE-INGESTION - THE ROLE OF TUMOR-NECROSIS-FACTOR-ALPHA

BACKGROUND. Previous studies have demonstrated an increased basal meta bolic rate in cancer patients. However, no previous study has investig ated the changes in energy expenditure and substrate oxidation after a dministration of a glucose load. Furthermore, the role of tumor necros is factor-alpha (TNF-alpha) on cancer-induced metabolic changes is sti ll a neglected area. METHODS, In 25 cancer patients and 16 healthy sub jects matched with regard to age, body mass index, and fat-free mass, indirect calorimetry was made before and after administration of a glu cose load (75 g per subject, administered orally). RESULTS. Cancer pat ients had fasting plasma concentrations of insulin (74 +/- 3.3 vs. 67 +/- 4.1 pmol/L; P < 0.05), lactate (0.68 +/- 0.11 vs. 0.41 +/- 0.1 mmo l/L; P < 0.05), free fatty acids (884 +/- 121 vs. 342 +/- 76 mmol/mL; P < 0.001), and TNF-alpha (1.23 +/- 0.31 vs. 0.45 +/- 0.11 ng/mL; P < 0.01) greater than controls, whereas plasma glucose concentrations (4. 8 +/- 0.5 vs. 5.1 +/- 0.3 mmol/L; P = not significant) were not differ ent from controls. Indirect calorimetry at baseline demonstrated that basal metabolic rate, fat oxidation, and protein oxidation were signif icantly greater in cancer patients than in controls. After administrat ion of the glucose load, carbohydrate oxidation progressively rose in both cancer patients and controls, with no differences between the two groups, whereas glucose uptake (59.3 +/- 3.8 vs. 69.1 +/- 3.6 g/kg fa t-free mass [FFM] x 240 minutes; P < 0.01) and storage (49.1 +/- 4.1 v s. 60.2 +/- 3.3 g/kg FFM x 240 minutes; P < 0.05) were markedly reduce d in cancer patients as compared with controls. Finally, glucose-induc ed thermogenesis (GIT) was lower in cancer patients than in controls. CONCLUSIONS. This study demonstrated that GIT is lower in cancer patie nts than in healthy subjects matched with regard to age and body mass index An overacti vity of the glucose fatty acid cycle is responsible for such results. Plasma concentrations of TNF-alpha might play a modu lating role in the metabolic changes that occur after administration o f a glucose load. The role of TNF-alpha on glucose and lipid metabolis m in cancer patients would be a worthy subject of future investigation s. (C) 1997 American Cancer Society.