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链脲佐菌素诱导的糖尿病大鼠经体内胰岛素治疗后胰腺生长抑素分泌异常得到纠正。

Abnormalities of pancreatic somatostatin secretion corrected by in vivo insulin treatment of streptozotocin-diabetic rats.

作者信息

Trimble E R, Gerber P P, Renold A E

出版信息

Diabetes. 1981 Oct;30(10):865-7. doi: 10.2337/diab.30.10.865.

Abstract

In islets removed from untreated streptozotocin-diabetic rats, the somatostatin-containing cells were unresponsive to changes in glucose concentration, while they did respond to raised cyclic AMP levels. By contrast, in vivo insulin treatment restored the glucose sensitivity of the somatostatin secreting cells. In addition, in vivo insulin treatment resulted in a lowering of the high basal somatostatin secretion rate found in islets from untreated diabetic rats. These changes were made without any alteration of islet insulin content or enhancement of the in vitro insulin secretion. These results indicate that there is not a basic defect in the glucoreceptor of the somatostatin cell in diabetes.

摘要

在从未经治疗的链脲佐菌素诱导的糖尿病大鼠中取出的胰岛中,含生长抑素的细胞对葡萄糖浓度的变化无反应,而它们对升高的环磷酸腺苷水平有反应。相比之下,体内胰岛素治疗恢复了生长抑素分泌细胞的葡萄糖敏感性。此外,体内胰岛素治疗导致未治疗的糖尿病大鼠胰岛中高基础生长抑素分泌率降低。这些变化并未改变胰岛胰岛素含量或增强体外胰岛素分泌。这些结果表明,糖尿病中生长抑素细胞的葡萄糖受体不存在基本缺陷。

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