Lutz T A, Tschudy S, Rushing P A, Scharrer E
Institute of Veterinary Physiology, University of Zürich, Winterthurerstrasse 260, CH-8057 Zurich, Switzerland.
Physiol Behav. 2000 Sep 15;70(5):533-6. doi: 10.1016/s0031-9384(00)00302-4.
Previous studies provided evidence for an interaction between the satiety effects of cholecystokinin (CCK), bombesin (BBS), and amylin. Amylin released in response to CCK (or BBS) was supposed to mediate part of CCK's (or BBS's) anorectic effect since the amylin and calcitonin gene-related peptide (CGRP) antagonist CGRP 8-37 attenuated their anorectic action. Due to the low specificity of CGRP 8-37 for amylin vs. CGRP binding sites, the aim of the present study was to test whether the specific amylin antagonist AC 253 also influenced the anorectic effects of CCK and BBS. Injections took place at dark onset in 24-h food-deprived rats. At a dose that attenuated the anorectic effect of amylin (5 microg/kg), the amylin antagonist AC 253 (500 microg/kg) significantly attenuated the anorectic effects of CCK and BBS (0.5 microg/kg). It can therefore be concluded that amylin, rather than CGRP, mediates part of the anorectic effects of CCK and BBS.
先前的研究为胆囊收缩素（CCK）、蛙皮素（BBS）和胰淀素的饱腹感效应之间存在相互作用提供了证据。由于CCK（或BBS）刺激释放的胰淀素被认为介导了CCK（或BBS）部分的厌食作用，因为胰淀素和降钙素基因相关肽（CGRP）拮抗剂CGRP 8-37减弱了它们的厌食作用。鉴于CGRP 8-37对胰淀素与CGRP结合位点的特异性较低，本研究的目的是测试特异性胰淀素拮抗剂AC 253是否也会影响CCK和BBS的厌食作用。在24小时禁食的大鼠中，于黑暗开始时进行注射。在能减弱胰淀素厌食作用的剂量（5微克/千克）下，胰淀素拮抗剂AC 253（500微克/千克）显著减弱了CCK和BBS（0.5微克/千克）的厌食作用。因此可以得出结论，介导CCK和BBS部分厌食作用的是胰淀素，而非CGRP。
