Somatostatin analogs inhibit somatostatin release.

Somatostatin analogs inhibit somatostatin release.
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生长抑素类似物抑制生长抑素释放。

DOI:
10.1210/endo-104-5-1270
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发表时间:
1979
期刊:
影响因子:
4.8
通讯作者:
R. Unger
R. Unger
中科院分区:
医学2区
文献类型:
--
作者:
E. Ipp;J. Rivier;R. Dobbs;Marvin R. Brown;W. Vale;R. Unger

文献摘要

被引文献

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为了确定生长抑素是否像胰岛素一样抑制其自身从胰腺的分泌,使用非循环系统将生长抑素的无免疫反应类似物灌注到离体狗胰十二指肠制剂中。[D-Trp8-D-Cys14] 200 ng/ml浓度的生长抑素可阻断生长抑素样免疫反应(SLI)对胆囊收缩素和精氨酸的反应。停止类似物灌注后,SLI释放增加。在0.1 ng/ml浓度下,des Asn5-[D-Trp8]生长抑素显著降低SLI水平,但未显著降低胰高血糖素水平。在浓度为1 ng/ml时,des Asn5-[D-Trp8]生长抑素显著抑制SLI以及胰岛素和胰高血糖素的释放。灌注浓度为10 ng/ml的胰高血糖素未能克服50 ng/ml des Asn5-[D-Trp8]生长抑素对SLI和胰岛素释放的阻断。该结果与生长抑素类似物对SLI释放的直接抑制作用相一致,并提出了天然激素自我抑制作用的可能性。
To determine if, like insulin, somatostatin inhibits its own secretion from the pancreas, nonimmunoreactive analogs of somatostatin were perfused in an isolated dog pancreaticoduodenal preparation using a nonrecirculating system. [D-Trp8-D-Cys14]somatostatin, at a concentration of 200 ng/ml, blocked the response of somatostatin-like immunoreactivity (SLI) to cholecystokinin and arginine. When perfusion of the analog was discontinued, SLI release increased. At a concentration of 0.1 ng/ml, des Asn5-[D-Trp8]somatostatin lowered SLI levels significantly without significantly reducing glucagon levels. At a concentration of 1 ng/ml, des Asn5-[D-Trp8]somatostatin significantly inhibited SLI as well as insulin and glucagon release. Perfusion of glucagon at a concentration of 10 ng/ml failed to overcome the blockade of SLI and insulin release caused by 50 ng/ml des Asn5-[D-Trp8]somatostatin. The results are compatible with a direct inhibitory effect of somatostatin analogs upon SLI release and raise the possibility of a self-inhibiting action of the native hormone.