Glucose and urea kinetics in patients with early and advanced gastrointestinal cancer: the response to glucose infusion, parenteral feeding, and surgical resection.
Glucose and urea kinetics in patients with early and advanced gastrointestinal cancer: the response to glucose infusion, parenteral feeding, and surgical resection.
复制标题
早期和晚期胃肠癌患者的葡萄糖和尿素动力学：对葡萄糖输注、肠外喂养和手术切除的反应。
作者：
J. H. Shaw;R. Wolfe
我们用同位素测定了正常志愿者（n = 16）、早期胃肠道（EGI）癌患者（n = 6）和晚期胃肠道（AGI）癌患者（n = 10）的葡萄糖周转率、尿素周转率和葡萄糖氧化率。在基础状态、葡萄糖输注（4 mg/kg/min）期间和全胃肠外喂养期间（仅AGI癌症患者）进行研究。在癌症切除术后2至3个月，还研究了早期疾病患者。志愿者和EGI癌症患者的基础葡萄糖转换率相似（分别为13.9 +/- 0.3 mumol/kg/min和13.3 +/- 0.2 mumol/kg/min），但AGI癌症患者的基础葡萄糖转换率显著较高（17.6 +/- 1.4 mumol/kg/min）。葡萄糖输注导致两个患者组中内源性产生的抑制显著低于志愿者（EGI组为76% +/- 6%，AGI组为69% +/- 7%，志愿者为94% +/- 4%）。葡萄糖氧化速率与肿瘤体积成比例地进行性增加。在志愿者中，葡萄糖氧化产生的VCO 2百分比为23.9% +/-0.7%，EGI和AGI组的值分别为32.8% +/- 2.0%和43.0% +/-3.0%。肿瘤根治性切除后，葡萄糖利用率显著降低（p <0.05）。AGI组的尿素周转率（8.4 +/- 1.0 mumol/kg/min）显著高于志愿者组的5.9 +/- 0.6 mumol/kg/min（p <0.03）。葡萄糖输注导致志愿者的尿素周转显著抑制（p <0.02），但AGI组葡萄糖输注未诱导统计学显著降低。我们从这些研究中得出结论，即使是一个小的，潜在的可治愈的胃肠道癌症的存在与正常的主机调节机制，旨在保护身体资源的损失;这种影响是更显着的肿瘤体积增加;增加肿瘤体积的影响葡萄糖利用和蛋白质分解的逐步增加。
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 mumol/kg/min and 13.3 +/- 0.2 mumol/kg/min, respectively) but were significantly higher in patients with AGI cancer (17.6 +/- 1.4 mumol/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 less than 0.05). The rate of urea turnover was significantly higher in the AGI group (8.4 +/- 1.0 mumol/kg/min) in comparison with the volunteer group value of 5.9 +/- 0.6 mumol/kg/min (p less than 0.03). Glucose infusion resulted in a significant suppression of urea turnover in the volunteers (p less than 0.02), but in the AGI group glucose infusion did not induce a statistically significant decrease. We conclude from these studies that 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; this effect is more marked as the tumor bulk increases; increasing tumor bulk effects a progressive increase in glucose utilization and in protein breakdown.