BLOCKADE OF TYPE-A, NOT TYPE-B, CCK RECEPTORS ATTENUATES SATIETY ACTIONS OF EXOGENOUS AND ENDOGENOUS CCK
BLOCKADE OF TYPE-A, NOT TYPE-B, CCK RECEPTORS ATTENUATES SATIETY ACTIONS OF EXOGENOUS AND ENDOGENOUS CCK
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DOI：
10.1152/ajpregu.1992.262.1.r46
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发表时间：
1992-01-01
影响因子：
--
通讯作者：
MCHUGH, PR
中科院分区：
文献类型：
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作者：
MORAN, TH;AMEGLIO, PJ;MCHUGH, PR
最近的研究表明，作用于A型或B型CCK受体的内源性胆囊收缩素（CCK）的释放在控制食物摄入中起作用。为了研究外源性给药和内源性释放的CCK抑制食物摄入的机制是否相似，是否依赖于与A型或B型CCK受体的相互作用，我们在大鼠中检测了A型细胞的能力，（L 364718）和B型（L 365260）CCK受体拮抗剂，用于1）阻断由腹膜内注射4 μ g/kg CCK产生的葡萄糖消耗抑制，和2）增加葡萄糖消耗的情况下，外源性CCK后6小时白天剥夺。增加A型CCK拮抗剂的剂量（10-100 μ g/kg）导致CCK产生的摄取抑制的剂量相关阻断，并且100 μ g/kg剂量的A拮抗剂显著增加葡萄糖摄取超过基线水平。相反，任何剂量（10- 1，000 μ g/kg）的B拮抗剂在任何时间点都不能阻断外源性CCK的抑制作用。在不存在外源性CCK的情况下，32和100 μ g/kg剂量的L 364718使摄入量增加至高于基线水平。B型拮抗剂L 365260的剂量（3.2-320 μ g/kg）不影响该范例中的摄入。这些结果表明，外源性和内源性CCK的摄食抑制作用的介导是相似的，并依赖于A型CCK受体的激活。
Recent work has suggested a role for an endogenous release of cholecystokinin (CCK) acting at either type A or type B CCK receptors in the control of food intake. In an effort to investigate whether the mechanisms by which exogenously administered and endogenously released CCK inhibits food intake are similar and depend upon interactions with either type A or type B CCK receptors, we examined in rats the ability of the type A (L 364718) and type B (L 365260) CCK receptor antagonists to 1) block the inhibition of glucose consumption produced by an intraperitoneal injection of 4-mu-g/kg of CCK and 2) increase glucose consumption in the absence of exogenous CCK after a 6-h daytime deprivation. Increasing dosages (10-100-mu-g/kg) of the type A CCK antagonist resulted in a dose-related blockade of the inhibition of intake produced by CCK, and the 100-mu-g/kg dose of the A antagonist significantly increased glucose intake above baseline levels. In contrast, no dose (10-1,000-mu-g/kg) of the B antagonist blocked the inhibitory action of exogenous CCK at any time point. In the absence of exogenous CCK, the 32 and 100-mu-g/kg doses of L 364718 increased intake above baseline levels. No dose (3.2-320-mu-g/kg) of the type B antagonist, L 365260, affected intake in this paradigm. These results suggest that the mediation of the feeding-inhibitory effects of exogenous and endogenous CCK are similar and depend upon activation of type A CCK receptors.