Jebbink M C, Jansen J B, Mooy D M, Schouten C M, Lamers C B
Department of Gastroenterology, University Hospital of Leiden, The Netherlands.
Peptides. 1992 Mar-Apr;13(2):287-90. doi: 10.1016/0196-9781(92)90110-o.
To determine whether exogenous cholecystokinin (CCK) inhibits endogenous CCK release, cholecystokinin-8S (CCK-8S) was infused intravenously during continuous intraduodenal stimulation of endogenous CCK by a meal. CCK was measured in plasma by 2 region-specific radioimmunoassays employing antibodies T204 and 1703. AB T204 binds to carboxy-terminal CCK peptides containing the sulphated tyrosyl region, including CCK-8S, and AB 1703 to carboxy-terminal CCK peptides containing at least 14 amino acid residues. Meal-stimulated plasma CCK concentrations remained elevated during the entire infusion period. CCK-8S infusion further increased meal-stimulated plasma CCK concentrations, when measured with AB T204, while meal-stimulated plasma CCK concentrations were not suppressed by CCK-8S infusion, when measured with AB 1703. It is concluded that meal-stimulated endogenous CCK release is not affected by the effects of intravenously administered CCK-8S. These data suggest that autocrine feedback regulation of CCK release is not operative in man.
为了确定外源性胆囊收缩素（CCK）是否抑制内源性CCK释放，在通过进食持续十二指肠内刺激内源性CCK期间，静脉内输注八肽胆囊收缩素（CCK-8S）。采用抗体T204和1703的两种区域特异性放射免疫测定法测定血浆中的CCK。抗体T204与含硫酸化酪氨酰区域的羧基末端CCK肽结合，包括CCK-8S，而抗体1703与含至少14个氨基酸残基的羧基末端CCK肽结合。在整个输注期间，进食刺激的血浆CCK浓度持续升高。当用抗体T204测定时，CCK-8S输注进一步增加了进食刺激的血浆CCK浓度，而当用抗体1703测定时，CCK-8S输注并未抑制进食刺激的血浆CCK浓度。得出的结论是，进食刺激的内源性CCK释放不受静脉注射CCK-8S的影响。这些数据表明，CCK释放的自分泌反馈调节在人类中不起作用。
