Respective roles of CCK-A and B receptors in the regulation

胆囊收缩素（CCK）是一种重要的胃肠激素和神经递质。已经确定了两种类型的CCK受体（A型和B型）。已知CCK-A受体与饱腹感、食物摄入和行为有关，而B受体与焦虑有关。我们最近饲养了CCK-A， -B和AB受体敲除小鼠，确定了这些受体的作用。CCK-BR（-/-）和AR(-/-)BR（-/-）小鼠与CCK-AR(+/+)BR（+/+）和AR（-/-）小鼠相比，焦虑状态增加。既往报道显示，CCK-4可诱导惊恐发作和焦虑，CCK-4主要结合CCK-BR。我们的观察与以前的报告不一致。进一步的研究是必要的。CCK BR（-/-）和CCK- ar (-/-)BR（-/-）小鼠的日能量摄入和能量消耗显著高于CCK- ar（-/-）和野生型[CCKAR(+/+)BR(+/+)]小鼠。CCKAR(-/-)BR（-/-）组小鼠每体重（g-kg）的肝脏和肾脏比例显著高于野生型小鼠。在CCK-BR基因破坏的情况下，能量代谢和能量周转增加，但真正的机制尚不清楚。CCK-AR（-/-）小鼠胃排空未延迟。CCK-BR（-/-）和AR(-/-)BR（-/-）小鼠胃排空增强。然而，给药阿托品显著抑制胃排空在所有小鼠。CCK-8对CCK-AR(+/+)BR（+/+）和BR（-/-）小鼠胃排空有延迟作用，但对CCK-AR（-/-）和AR(-/-)BR（-/-）小鼠无延迟作用。在小鼠中，CCK、乙酰胆碱和GRP能刺激胰腺淀粉酶释放，而只有CCK能诱导胆囊阶梯收缩。

Cholecystokinin (CCK) is an important gastrointestinal hormone as well as neurotransmitter. Two types of CCK receptors (type A and type B) have been identified. The CCK-A receptor is known to be involved in satiety, food intake and behavior and the B receptor to be involved in anxiety. As we recently raised CCK-A, -B and AB receptor knockout mice, the role of these receptors was determined.CCK-BR(-/-) and AR(-/-)BR(-/-) mice showed increased anxiety states compared with CCK-AR(+/+)BR(+/+) and AR(-/-) mice. Previous reports showed that panic attack and anxiety could be induced by CCK-4, which predominantly bound CCK-BR. Our observation was not compatible for the previous report. Further study is necessary.The daily energy intake and energy expenditure were significantly higher in CCK BR(-/-) and CCK-AR(-/-)BR(-/-) mice than CCK-AR(-/-) and wild-type [CCKAR(+/+)BR(+/+)] mice. The ratios of liver and kidneys per body weight (g-kg) were significantly higher in CCKAR(-/-)BR(-/-) mice than wild-type mice. Energy metabolism and energy turnover were increased under the condition of disruption of CCK-BR gene, although the real mechanism is unknown.Gastric emptying was not delayed in CCK-AR(-/-) mice. Gastric emptying was enhanced in CCK-BR(-/-) and AR(-/-)BR(-/-) mice. However, administration of atropine significantly inhibited gastric emptying in all mice. CCK-8 delayed gastric emptying in CCK-AR(+/+)BR(+/+) and BR(-/-) mice, but not in CCK-AR(-/-) and AR(-/-)BR(-/-) mice.In mice, CCK, acetylcholine, and GRP could stimulate amylase release from the pancreas, whereas only CCK could induce gallb ladder contration.