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

CCK是一种重要的胃肠激素，也是一种神经递质。CCK受体有两种类型(A型和B型)。众所周知，CCK-A受体与饱腹感、食物摄取和行为有关，B受体与焦虑有关。随着我们最近培育CCK-A、-B和AB受体基因敲除小鼠，这些受体的作用被确定。与CCK-AR(/)BR(/)和AR(-/-)小鼠相比，CCK-BR(-/-)和AR(-/-)BR(-/-)小鼠表现出更高的焦虑状态。以前的报道表明，CCK-4可以引起惊恐发作和焦虑，CCK-4主要与CCK-BR结合。我们的观察结果与前一份报告不符。CCK-AR(-/-)和CCK-AR(-/-)BR(-/-)小鼠的每日能量摄入量和能量消耗显著高于CCK-AR(-/-)和野生型[CCK-AR(/)BR(/)]小鼠。CKAR(-/-)BR(-/-)小鼠肝肾比(g-kg)显著高于野生型小鼠。CCK-BR基因突变可促进能量代谢和能量周转，但其机制尚不清楚，CCK-AR(-/-)小鼠的胃排空未受影响。CCK-BR(-/-)和AR(-/-)BR(-/-)小鼠的胃排空功能增强。然而，给予阿托品显著抑制了所有小鼠的胃排空。CCK-8可使CCK-AR(/)BR(/)和BR(-/-)小鼠胃排空延迟，但对CCK-AR(-/-)和AR(-/-)BR(-/-)小鼠无明显影响。在小鼠中，CCK、乙酰胆碱和GRP能刺激胰脏淀粉酶释放，而只有CCK能引起胆汁阶梯收缩。

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.