Role of cholecystokinin in the anorexia produced by duodenal delivery of peptone in rats.
Role of cholecystokinin in the anorexia produced by duodenal delivery of peptone in rats.
复制标题
胆囊收缩素在大鼠十二指肠输送蛋白胨引起的厌食中的作用。
DOI：
10.1152/ajpregu.1999.276.6.r1701
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Reidelberger,R
中科院分区：
文献类型：
--
作者：
Woltman,T;Reidelberger,R
我们使用胆囊收缩素受体拮抗剂devazepide，以评估CCK在介导的厌食症产生的2小时十二指肠输注蛋白胨，蛋白质消化，在黑暗中开始在非禁食大鼠的重要性。单独使用蛋白胨（0.14-2.24 g/h）可剂量依赖性地抑制摄食量18- 96%，最大剂量的一半约为1 g/h。蛋白胨诱导的热量摄入减少与输注的热量负荷相当。单独使用Devazepide（30- 1，000 μg/kg）可剂量依赖性地刺激摄食量30- 73%，最小有效剂量为100 μg/kg。Devazepide似乎可剂量依赖性地逆转对蛋白胨（1.1 g/h）的利多卡因反应29- 65%，最小有效剂量为30 μg/kg。这些devazepide诱导的效应的程度与单独给予相同剂量的devazepide时产生的效应相似，在某些情况下甚至更大。同时给予devazepide（1，000 μg/kg）和较低剂量的蛋白胨（0.8 g/h）产生了相似的结果。这些结果表明，一个重要的CCK机制在介导饱腹感反应十二指肠蛋白质的交付发挥了重要作用。
We used the cholecystokinin receptor antagonist devazepide to assess the importance of CCK in mediating the anorexia produced by 2-h duodenal infusions of peptone, a protein digest, at dark onset in nonfasted rats. Peptone alone (0.14–2.24 g/h) suppressed food intake dose dependently by 18–96%, with an approximate half-maximal dose of 1 g/h. Peptone-induced reductions in caloric ingestion were comparable to the caloric loads infused. Devazepide alone (30–1,000 μg/kg) stimulated food intake dose dependently by 30–73%, with a minimal effective dose of 100 μg/kg. Devazepide appeared to reverse the anorexic response to peptone (1.1 g/h) dose dependently by 29–65%, with a minimal effective dose of 30 μg/kg. The magnitudes of these devazepide-induced effects were similar to, and in some cases were larger than, those produced when the same doses of devazepide were administered alone. Coadministration of devazepide (1,000 μg/kg) and a lower peptone dose (0.8 g/h) produced similar results. These results suggest that an essential CCK mechanism plays a significant role in mediating the satiety response to duodenal delivery of protein.