Frankel B J, Sehlin J
Department of Histology and Cell Biology, University of Umeå, Sweden.
Pancreas. 1994 Sep;9(5):550-7. doi: 10.1097/00006676-199409000-00002.
Insulin release and 45Ca2+ uptake were studied in isolated islets from Chinese hamsters of genetically diabetic and normal sublines. The calcium channel agonist, perchlorate (ClO4-, 12 mmol/L), augmented both 45Ca2+ uptake and insulin release from normal islets in the presence of 20 but not 1 mmol/L glucose. The agonist also amplified the glucose-stimulated 45Ca2+ uptake and insulin release from diabetic islets but did not normalize the insulin release despite normal insulin concentration in the diabetic Chinese hamster islets. The dry weight of the diabetic islets was subnormal (54%, p < 0.005) but the insulin concentration (insulin per dry weight of islet tissue) was not different from normal (122%). It appears that there are defective mechanisms in addition to the glucose-stimulated influx of Ca2+ in diabetic islet B cells.
对遗传性糖尿病和正常亚系中国仓鼠的分离胰岛中的胰岛素释放和45Ca2+摄取进行了研究。钙通道激动剂高氯酸盐（ClO4-，12 mmol/L）在20 mmol/L而非1 mmol/L葡萄糖存在的情况下，增强了正常胰岛的45Ca2+摄取和胰岛素释放。该激动剂还放大了糖尿病胰岛的葡萄糖刺激的45Ca2+摄取和胰岛素释放，但尽管糖尿病中国仓鼠胰岛中的胰岛素浓度正常，却未能使胰岛素释放正常化。糖尿病胰岛的干重低于正常水平（54%，p < 0.005），但胰岛素浓度（每胰岛组织干重的胰岛素）与正常水平无差异（122%）。看来，除了葡萄糖刺激的Ca2+流入外，糖尿病胰岛B细胞中还存在缺陷机制。
