胆囊收缩素（CCK）-33刺激灌流大鼠胰腺分泌胰岛素：结构-活性关系研究

Cholecystokinin (CCK)-33 stimulates insulin secretion from the perfused rat pancreas: studies on the structure-activity relationship.

作者信息

Sandberg E, Ahrén B, Tendler D, Efendic S

机构信息

Department of Endocrinology, Karolinska Institutet, Stockholm, Sweden.

出版信息

Pharmacol Toxicol. 1988 Jul;63(1):42-5. doi: 10.1111/j.1600-0773.1988.tb00907.x.

DOI:10.1111/j.1600-0773.1988.tb00907.x

PMID:3041399

Abstract

Cholecystokinin (CCK)-33 is known to stimulate insulin secretion. Presently, using the perfused rat pancreas, we have characterized the active site in the CCK-33 molecule that is responsible for this effect by the use of different CCK fragments. We found that CCK-33, CCK-8 and CCK-7 (1 nM) all significantly stimulated insulin secretion in the presence of 4.4 mM or 6.7 mM glucose. However, CCK-7 was much less potent than the longer forms. In contrast, CCK-4, CCK-6 and CCK-33 (1-21) had no effect on insulin secretion. We conclude that the shortest CCK-form that stimulates insulin secretion at 1 nM is the C-terminal heptapeptide CCK-7. However, CCK-8 is much more potent than CCK-7 in this respect.

摘要

已知胆囊收缩素（CCK）-33能刺激胰岛素分泌。目前，我们利用灌注大鼠胰腺，通过使用不同的CCK片段，对CCK-33分子中负责此效应的活性位点进行了表征。我们发现，在存在4.4 mM或6.7 mM葡萄糖的情况下，CCK-33、CCK-8和CCK-7（1 nM）均能显著刺激胰岛素分泌。然而，CCK-7的效力远低于较长形式的CCK。相比之下，CCK-4、CCK-6和CCK-33（1-21）对胰岛素分泌没有影响。我们得出结论，在1 nM时刺激胰岛素分泌的最短CCK形式是C末端七肽CCK-7。然而，在这方面CCK-8比CCK-7的效力要强得多。