Infusion of CCK-8 into hepatic-portal vein fails to reduce food intake in rats.
Infusion of CCK-8 into hepatic-portal vein fails to reduce food intake in rats.
复制标题
将CCK-8输注到肝门静脉中并不能减少大鼠的食物摄入量。
DOI：
10.1152/ajpregu.1987.252.5.r1015
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Gibbs,J
中科院分区：
文献类型：
--
作者：
Greenberg,D;Smith,GP;Gibbs,J
如果内源性胆囊收缩素(CCK)的饱和效应是通过循环激素机制产生的，那么将外源性CCK注入肝-门静脉应该会减少进食量。为了验证这一点，一种形式的内源性CCK，C末端八肽CCK-8，在试验餐之前按4微克/公斤和8微克/公斤的剂量注入门脉内。这两种剂量都不会减少门静脉输注后的食物摄入量，即使在相同的大鼠中，腹腔注射4微克/公斤CCK-8会减少大约50%的进食量。这些结果表明，如果内源性CCK-8具有饱腹感，它主要通过旁分泌机制起作用。
If the putative satiating effect of endogenous cholecystokinin (CCK) is produced through a circulating hormonal mechanism, then administration of exogenous CCK into the hepatic-portal vein should decrease meal size. To test this, one form of endogenous CCK, the C-terminal octapeptide CCK-8, was infused intraportally in doses of 4 and 8 micrograms/kg just prior to a test meal. Neither dose decreased food intake after intraportal infusion even though intraperitoneal administration of 4 micrograms/kg CCK-8 decreased meal size approximately 50% in the same rats. The results suggest that if endogenous CCK-8 has a satiating effect, it acts primarily through a paracrine mechanism.