Rehfeld J F
J Clin Invest. 1976 Jul;58(1):41-9. doi: 10.1172/JCI108457.
The insulin and gastrin response to oral glucose, intravenous glucose, or a protein-rich meal were measured in 44 nondiabetic patients with pernicious anemia (PA) and in 44 control subjects. 36 of the PA-patients had hypergastrinemia, while serum gastrin concentrations in the remaining eight patients were below normal. Three hypergastrinemic PA-patients were in addition studied during an oral glucose loading with synchronous intravenous infusion of gastrin-17. During both oral and intravenous glucose tests blood glucose concentrations were similar in patients and in controls. After ingestion of protein blood glucose concentrations in PA-patients with hypergastrinemia were above those of the controls (P less than 0.05). Parenteral infusion of gastrin-17 during oral glucose loading also increased blood glucose concentrations above the levels observed after glucose alone. In PA-patients with hypergastrinemia the insulin response was augmented in all tests. In patients with hypogastrinemia serum insulin concentrations were lower than normal in the fasting state and during stimulation with glucose intravenously (P less than 0.01). In hypergastrinemic patients serum gastrin concentrations decreased after oral as well as intravenous glucose administration. The decrease was larger during the oral test. In hypogastrinemia oral glucose induced, as in controls, a small initial rise followed by a slow fall in serum gastrin concentrations. No variations were seen in these patients during the intravenous glucose infusion. Gel filtration of serum from hypergastrinemic patients disclosed a decrease in the concentrations of all four main components of gastrin during the glucose loadings. Taken together with earlier studies on the effect of exogenous gastrin the results suggest that endogenous hypergastrinemia induces hyperglycemia and potentiates insulin secretion. In contrast hypogastrinemia is associated with hypoinsulinism.
对44例患有恶性贫血（PA）的非糖尿病患者和44例对照受试者测量了口服葡萄糖、静脉注射葡萄糖或富含蛋白质的餐食后的胰岛素和胃泌素反应。44例PA患者中有36例患有高胃泌素血症，而其余8例患者的血清胃泌素浓度低于正常水平。另外，对3例高胃泌素血症的PA患者在口服葡萄糖负荷试验期间同步静脉输注胃泌素-17进行了研究。在口服和静脉葡萄糖试验中，患者和对照组的血糖浓度相似。摄入蛋白质后，高胃泌素血症的PA患者的血糖浓度高于对照组（P<0.05）。口服葡萄糖负荷试验期间静脉输注胃泌素-17也使血糖浓度升高至单独葡萄糖试验后观察到的水平以上。在高胃泌素血症的PA患者中，所有试验中的胰岛素反应均增强。在低胃泌素血症患者中，空腹状态下和静脉注射葡萄糖刺激期间血清胰岛素浓度低于正常水平（P<0.01）。在高胃泌素血症患者中，口服和静脉注射葡萄糖后血清胃泌素浓度均降低。口服试验期间的降低幅度更大。在低胃泌素血症患者中，口服葡萄糖与对照组一样，最初血清胃泌素浓度有小幅度升高，随后缓慢下降。静脉输注葡萄糖期间这些患者未见变化。对高胃泌素血症患者的血清进行凝胶过滤显示，葡萄糖负荷试验期间胃泌素的所有四种主要成分浓度均降低。结合早期关于外源性胃泌素作用的研究结果表明，内源性高胃泌素血症会导致高血糖并增强胰岛素分泌。相比之下，低胃泌素血症与胰岛素分泌不足有关。
