CCK receptor function contribution and the gene expression regulation which affect eating, digestive organ capacity adaptation and life habit disease : Deliberation by human and CCK-A, B, AB receptor gene targeting mice.

胆囊收缩素（CCK）是一种具有重要生理功能的肽类激素。近年来，CCK-A和-B受体（R）被克隆。已经报道了胰腺CCK受体表达的种属差异。胆囊中有胆囊收缩素受体基因表达，胰腺中无胆囊收缩素受体基因表达。在包括人类在内的哺乳动物中，CCK通过CCK-AR介导饱腹感效应。我们研究了在CCK-AR、BR和ARBR基因敲除小鼠中，非营养性液体负荷的胃排空是否被改变。与野生型和CCK-AR（-/-）小鼠相比，缺乏CCK-BR的小鼠胃排空显著增强。CCK-8 S抑制CCK-AR小鼠的胃排空，但不抑制CCK-AR小鼠的胃排空。质子泵抑制剂不影响胃排空。阿托品剂量依赖性抑制胃排空在所有基因型。所有基因型的平滑肌厚度相当。在没有CCK-BR的小鼠中，非营养液体负荷的胃排空增强，尽管精确的胃排空率与CCK-BR的胃排空率无关。 关于我们 机制不明。虽然胆囊收缩素（CCK）已被证明通过CCK-A受体（CCK-ARs）抑制胃排空，但CCK-B受体（CCK-BRs）的作用尚未得到证实。我们研究了CCK-AR、BR和ARBR基因敲除小鼠的非营养性液体负荷胃排空是否发生改变，我们制备了CCK-AR基因缺陷（-/-）小鼠，发现与野生型小鼠相比，每日食物摄入量、能量消耗和液体餐胃排空没有变化。由于CCK-AR（-/-）小鼠表现出抗焦虑状态，我们检查了游泳应激或束缚应激后每日摄食量的变化。5分钟游泳3天并没有改变两种基因型之间的体重和每日食物摄入量的变化。7小时束缚应激显着降低体重，以及在随后的3天的食物摄入量。然后，在第四天，两种基因型的食物摄入量增加。CCK-AR（-/-）小鼠表现出明显高于束缚应激前的水平。然而，野生型小鼠的摄食量仅恢复到应激前的水平。提示CCK-AR功能可能参与应激性摄食亢进。少

Cholecystokinin(CCK) is a peptide hormone that has important physiological functions. Recently, CCK-A and -B receptor(R)s were cloned. Species differences in the pancreatic expression of CCK-Rs have been reported. Gene expression of CCK-AR was detected in human gallbladder, but not in human pancreas. In mammals including humans, CCK mediates satiety effect via CCK-AR. We examined whether gastric emptying of a nonnutrient liquid load was modified in CCK-AR, BR, and ARBR gene knockout mice. Gastric emptying was significantly enhanced in mice lacking CCK-BR, as compared with wild-type and CCK-AR(-/-) mice. CCK-8S inhibited gastric emptying in mice with CCK-AR, but not in mice without CCK-AR. A proton pump inhibitor did not affect gastric emptying. Atropine dose dependently inhibited gastric emptying in all genotypes. The thickness of smooth muscle was comparable for all genotypes. The gastric emptying of a nonnutrient liquid load was enhanced in mice without CCK-BR, although the precise m … More echanism is not known. Although cholecystokinin(CCK) has been shown to inhibit gastric emptying via CCK-A receptors(CCK-ARs), the role of CCK-B receptors(CCK-BRs) has not been verified. We examined whether gastric emptying of a nonnutrient liquid load was modified in CCK-AR, BR, and ARBR gene knockout mice.We generated CCK-AR gene deficient(-/-) mice and found that the daily food intake, energy expenditure, and gastric emptying of a liquid meal were not changed, compared with wild-type mice. As CCK-AR(-/-) mice showed a anxiolytic status, we examined the changes in daily food intake after the swimming stress or after the restraint stress. Five-minute swimming for 3 days did not modify the changes in body weight and daily food intake between the two genotypes. Seven-h restraint stress significantly decreased body weight as well as food intake during subsequent 3 days. Then, on the fourth day, food intake increased in both genotypes. CCK-AR(-/-) mice showed a significantly higher level than the value before restraint stress. However, the food intake was only recovered to the level before the stress in wild-type mice. This evidence suggested that the CCK-AR function might be involved in stress-induced hyperphagia. Less