Vinik A I, Kalk W J, Botha J L, Jackson W P, Blake K C
Diabetes. 1976 Jan;25(1):11-5. doi: 10.2337/diab.25.1.11.
Repeated intensive pancreatic beta-cell stimulation was carried out in 42 subjects, comprising 22 normal controls, 10 mild to "severe" maturity-onset diabetics, and 10 chronic pancreatitis patients. Each subject received 75 gm. oral glucose twice and 1 mg. glucagon plus 0.5 gm. tolbutamide intravenously three times at short intervals. Each of the three combined stimuli caused almost equivalent marked spikes of insulin release in all experimental groups. The total calculated output of insulin was equivalent to the total daily insulin output in normal subjects. Pancreatitics and those with severe diabetes (fasting blood sugar greater than 120 mg./100 ml.) had qualitatively similar but a quantitatively smaller response. Those with mild diabetes were similar to the normal subjects but had an exaggerated response to the second oral glucose dose, suggesting overactivity of the enteroinsular axis. Despite the inordinate insulin levels, hypoglycemia did not occur.
对42名受试者进行了反复强化的胰腺β细胞刺激实验,其中包括22名正常对照者、10名轻度至“重度”成年发病型糖尿病患者和10名慢性胰腺炎患者。每位受试者短时间内口服两次75克葡萄糖,静脉注射三次1毫克胰高血糖素加0.5克甲苯磺丁脲。在所有实验组中,三种联合刺激中的每一种都引起了几乎相当的明显胰岛素释放峰值。计算得出的胰岛素总输出量与正常受试者的每日胰岛素总输出量相当。胰腺炎患者和重度糖尿病患者(空腹血糖大于120毫克/100毫升)在质量上有相似的反应,但数量上较小。轻度糖尿病患者与正常受试者相似,但对第二次口服葡萄糖剂量反应过度,提示肠胰岛轴过度活跃。尽管胰岛素水平过高,但并未发生低血糖。