人血清中可引起胆囊收缩的非胆囊收缩素肽。

Noncholecystokinin peptides in human serum which cause gallbladder contraction.

作者信息

Cox K L, Rosenquist G L, Iwahashi-Hosoda C K

出版信息

Life Sci. 1982 Dec 27;31(26):3023-9. doi: 10.1016/0024-3205(82)90070-4.

Abstract

In fasting human serum, cholecystokinin (CCK) is not the principal substance which causes in vitro rabbit gallbladder contraction. Removal of CCK by affinity chromatography from fasting sera from 8 healthy adults reduced bioactivity only by 18 +/- 4% (SEM). Unlike CCK, the bioactivity of serum was enhanced by 30 to 57% rather than destroyed by pronase and chymotrypsin respectively and was not inhibited by dibutyryl cGMP. Reduction of serum bioactivity by carboxypeptidase Y indicated that the bioactive substances in serum are peptides. On Sephadex G-50, bioactive substances eluted in positions different from any known form of CCK. Thus, the principal substances in fasting human serum causing in vitro gallbladder contraction are not CCK but are most likely small peptides which act at receptors different from the receptors for CCK.

摘要

在空腹人体血清中，胆囊收缩素（CCK）并非引起体外兔胆囊收缩的主要物质。通过亲和层析从8名健康成年人的空腹血清中去除CCK后，生物活性仅降低了18±4%（标准误）。与CCK不同，血清的生物活性分别被链霉蛋白酶和胰凝乳蛋白酶增强了30%至57%，而非被破坏，且不受二丁酰环鸟苷酸抑制。羧肽酶Y降低血清生物活性表明血清中的生物活性物质是肽类。在葡聚糖凝胶G - 50上，生物活性物质在与任何已知形式的CCK不同的位置洗脱。因此，空腹人体血清中引起体外胆囊收缩的主要物质不是CCK，而很可能是作用于与CCK受体不同的受体的小肽。