Shichiri M, Kawamori R, Abe H
Diabetes. 1979 Apr;28(4):272-5. doi: 10.2337/diab.28.4.272.
Since it is important to elucidate the precise significance of pancreatic A-cell hypersecretion in the pathogenesis of diabetes mellitus, the change in the immunoreactive glucagon (IRG) response to 100 g oral glucose challenges was studied in diabetics whose blood glucose responses and plasma immunoreactive insulin concentrations (IRI) simulated those in normal subjects with the aid of the artificial beta cell system that we developed originally. In six nonobese adult-onset and four insulin-dependent diabetics whose blood glucose responses and plasma insulin concentrations after 100 g oral glucose load were made equivalent to those seen in normal subjects by the artificial beta cell, the glucagon release was similar to the response in normal subjects. In one insulin-dependent diabetic with high anti-insulin-binding capacity, the blood glucose response after an oral glucose challenge was not normalized by the artificial beta cell and the glucagon secretion was paradoxically increased. This fact suggested that the paradoxic rise in glucagon, seen in response to an oral glucose load in some diabetics, is secondary to insulin deficiency.
由于阐明胰岛A细胞分泌过多在糖尿病发病机制中的精确意义非常重要，我们利用最初开发的人工β细胞系统，对血糖反应和血浆免疫反应性胰岛素浓度（IRI）模拟正常受试者的糖尿病患者，研究了其对100g口服葡萄糖刺激的免疫反应性胰高血糖素（IRG）反应的变化。在6名非肥胖成年发病型糖尿病患者和4名胰岛素依赖型糖尿病患者中，通过人工β细胞使他们在100g口服葡萄糖负荷后的血糖反应和血浆胰岛素浓度与正常受试者相当，这些患者的胰高血糖素释放与正常受试者的反应相似。在1名具有高抗胰岛素结合能力的胰岛素依赖型糖尿病患者中，口服葡萄糖刺激后的血糖反应未通过人工β细胞恢复正常，且胰高血糖素分泌反而增加。这一事实表明，在一些糖尿病患者中，口服葡萄糖负荷后出现的胰高血糖素反常升高是胰岛素缺乏的继发表现。
