Glucose and urea kinetics in patients with early and advanced gastrointestinal cancer: the response to glucose infusion, parenteral feeding, and surgical resection
Shaw, J.H.; Wolfe, R.R.
Surgery 101(2): 181-191
1987
ISSN/ISBN: 0039-6060 PMID: 3101215 Document Number: 304822
We isotopically determined rates of glucose turnover, urea turnover, and glucose oxidation in normal volunteers (n=16), patients with early gastrointestinal (EGI) cancer (n=6), and patients with advanced gastrointestinal (AGI) cancer (n=10). Studies were performed in the basal state, during glucose infusion (4 mg/kg/min), and during total parenteral feeding (patients with AGI cancer only). Patients with early stages of the disease were also studied 2 to 3 months after resection of the cancer. Basal rates of glucose turnover were similar in volunteers and in patients with EGI cancer (13.9 .+-. 0.3 .mu.mol/kg/min and 13.3 .+-. 0.2 .mu.mol/kg/min, respectively) but were significantly higher in patients with AGI cancer (17.6 .+-. 1.4 .mu.mol/kg/min). Glucose infusion resulted in significantly less suppression of endogenous production in both patient groups than that seen in the volunteers (76% .+-. 6% for EGI group, 69% .+-. 7% for AGI group, and 94% .+-. 4% for volunteers). The rate of glucose oxidation increased progressively in proportion to the tumor bulk. In the volunteers the percent of VCO2 from glucose oxidation was 23.9% .+-. 0.7%, and in EGI and AGI groups the values were 32.8% .+-. 2.0% and 43.0% .+-. 3.0%, respectively. After curative resection of the cancer, glucose utilization decreased significantly (p < 0.05). The rate of urea turnover was significantly higher in the AGI group (8.4 .+-. 1.0 .mu.mol/kg/min) in comparison with the volunteer group value of 5.9 .+-. 0.6 .mu.mol/kg/min (p < 0.03). Glucose infusion resulted in a significant suppression of urea turnover in the volunteers (p < 0.02), but in the AGI group glucose infusion did not induce a statistically significant decrease. We conclude from these studies that (1) the presence of even a small, potentially curable gastrointestinal cancer is associated with a loss of the normal host-regulatory mechanisms designed to conserve body resources; (2) this effect is more marked as the tumor bulk increases; (3) increasing tumor bulk effects a progressive increase in glucose utilization and in protein breakdown.