Insulin release from the isolated perfused rat pancreas containing insulinomata induced by streptozotocin and nicotinamide: effects of glucose and responses to tumor removal.
Insulin release from the isolated perfused rat pancreas containing insulinomata induced by streptozotocin and nicotinamide: effects of glucose and responses to tumor removal.
复制标题
链脲佐菌素和烟酰胺诱导的含有胰岛素瘤的分离灌注大鼠胰腺的胰岛素释放：葡萄糖的影响和对肿瘤去除的反应。
作者：
T. Kazumi;C. Sakamoto;A. Ohki;G. Yoshino;M. Otsuki;S. Baba
在体外灌流的大鼠胰腺中研究了由链脲佐菌素和烟酰胺诱导的胰岛细胞瘤切除前后胰岛素分泌对葡萄糖的反应动力学。此外，将肿瘤切除前后的胰岛素分泌分别与假手术前后的正常胰腺进行比较。因此，对两种胰腺制备物进行葡萄糖重复灌注。用8.4 mM葡萄糖灌注含有肿瘤的胰腺导致双相释放，其模式与正常胰腺相似。然而，无论是基础和刺激的胰岛素分泌的荷瘤胰腺大于任何胰腺的肿瘤已被排除结扎或那些正常胰腺假手术前。葡萄糖浓度从2.8到8.4 mM的第二次增加也产生了来自肿瘤外胰腺以及来自假手术正常胰腺的胰岛素的双相释放。而瘤外胰腺组织对葡萄糖的胰岛素分泌反应低于对照胰腺组织。我们的研究结果表明，由链脲佐菌素和烟酰胺诱导的胰岛细胞肿瘤对葡萄糖有典型的双相胰岛素释放反应。因此，化学诱导的大鼠胰岛素瘤可以提供一个容易获得的和有价值的模型的胰岛素分泌组织，类似于正常的胰岛。此外，我们的研究表明，含肿瘤的胰腺的B细胞功能受到预先存在的肿瘤诱导的高胰岛素血症或其代谢后果的抑制。
The kinetics of insulin secretion in response to glucose were studied in the in vitro perfused rat pancreas before and after removal of islet cell tumors induced by streptozotocin and nicotinamide. In addition, insulin secretion before and after tumor removal was compared with that from normal pancreata before and after sham operations, respectively. Thus, the two pancreas preparations were subjected to repeated perfusions with glucose. Perfusion of pancreata containing tumors with 8.4 mM glucose resulted in biphasic release in a pattern similar to that of normal pancreas. However, both basal and stimulated insulin secretion of tumor-bearing pancreata were greater than either those of pancreata from which tumors had been excluded by ligature or those of normal pancreata before sham operation. A second increase in the concentration of glucose from 2.8 to 8.4 mM also produced a biphasic release of insulin from extratumoral pancreata as well as from sham-operated normal pancreata. However, the insulin secretory response to glucose of extratumoral pancreatic tissue was less than that of control pancreatic tissue. Our findings indicate that pancreatic islet cell tumors induced by streptozotocin and nicotinamide respond to glucose with typical biphasic insulin release. Thus, chemically induced rat insulinomata may provide a readily available and valuable model of insulin-secreting tissue, analogous to normal islets. Furthermore, our study suggests that the B cell function of pancreata containing tumors is inhibited by the preexisting tumor-induced hyperinsulinism or by its metabolic consequences.