Schneider L H, Gibbs J, Smith G P
Peptides. 1986 Jan-Feb;7(1):135-40. doi: 10.1016/0196-9781(86)90073-2.
Proglumide, a selective antagonist of exogenous cholecystokinin in vitro, also inhibits the reduction of food intake induced by the systemic administration of cholecystokinin octapeptide (CCK-8) in food deprived rats. On the basis of an increase in the size of a brief test meal which followed an oral preload and treatment with a single dose of proglumide, it was suggested that a role for endogenous cholecystokinin in satiety had been demonstrated. We attempted to replicate this finding and could not under very similar experimental conditions. Subsequently, we tested whether other proglumide doses would antagonize the satiating effect of a larger oral preload on test meal intake. When these results were also found to be negative, we confirmed that proglumide (at several doses) significantly antagonized the reduction in food intake induced by exogenous CCK-8 under our conditions. Since proglumide antagonized the satiating effect of exogenous CCK-8, but did not increase food intake after oral preloads that were presumed to release endogenous CCK, we conclude that a reliable satiating effect of endogenous CCK remains to be demonstrated.
丙谷胺是一种体外外源性胆囊收缩素的选择性拮抗剂,它也能抑制在饥饿大鼠中通过全身注射八肽胆囊收缩素(CCK - 8)所诱导的食物摄入量减少。基于在口服预负荷后紧接着进行简短测试餐时,单剂量丙谷胺处理使测试餐量增加,有人提出内源性胆囊收缩素在饱腹感中起作用这一点已得到证实。我们试图重复这一发现,但在非常相似的实验条件下未能成功。随后,我们测试了其他丙谷胺剂量是否会拮抗更大口服预负荷对测试餐摄入量的饱腹感作用。当这些结果也被发现为阴性时,我们证实了在我们的实验条件下,丙谷胺(几种剂量)能显著拮抗外源性CCK - 8所诱导的食物摄入量减少。由于丙谷胺拮抗了外源性CCK - 8的饱腹感作用,但在假定能释放内源性CCK的口服预负荷后并没有增加食物摄入量,我们得出结论,内源性CCK可靠的饱腹感作用仍有待证实。