Enhanced gastric emptying of a liquid gastric load in mice lacking cholecystokinin-B receptor: a study of CCK-A,B, and AB receptor gene knockout mice

Enhanced gastric emptying of a liquid gastric load in mice lacking cholecystokinin-B receptor: a study of CCK-A,B, and AB receptor gene knockout mice
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DOI:
10.1007/s00535-003-1297-2
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发表时间:
2004-04
影响因子:
6.3
通讯作者:
K. Miyasaka;M. Ohta;S. Kanai;Y. Yoshida;Norikazu Sato;A. Nagata;T. Matsui;T. Noda;A. Jimi;S. Takiguchi;Y. Takata;T. Kawanami;A. Funakoshi
K. Miyasaka;M. Ohta;S. Kanai;Y. Yoshida;Norikazu Sato;A. Nagata;T. Matsui;T. Noda;A. Jimi;S. Takiguchi;Y. Takata;T. Kawanami;A. Funakoshi
中科院分区:
医学1区
文献类型:
--
作者:
K. Miyasaka;M. Ohta;S. Kanai;Y. Yoshida;Norikazu Sato;A. Nagata;T. Matsui;T. Noda;A. Jimi;S. Takiguchi;Y. Takata;T. Kawanami;A. Funakoshi

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背景胆囊收缩素(cholecystokinin,CCK)通过CCK-A受体(CCK-A receptor,CCK-ARs)抑制胃排空,但CCK-B受体(CCK-BRs)的作用尚不清楚。我们研究了是否胃排空的非营养液体负荷修改CCK-AR,BR,和ARBR基因敲除mice.MethodsA液体胃负荷准备与酚红通过口胃管(0.15毫升/小鼠)。通过断头处死动物,并在摄入后10和30 min估计胃排空。CCK-8的硫酸化形式(CCK-8 S)和阿托品的分级剂量的影响进行了检查。此外,质子泵抑制剂给药的野生型小鼠检查胃酸排空的贡献。ResultsGastric排空显着增强缺乏CCK-BR的小鼠,与野生型和CCK-AR(−/−)小鼠相比。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。平滑肌的厚度是可比的所有genotype.ConclusionsThe胃排空的nonnutritional液体负荷增强小鼠没有CCK-BR,虽然确切的机制是未知的。
BackgroundAlthough 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.MethodsA liquid gastric load prepared with phenol red was administered via an orogastric tube (0.15 ml/mouse). The animals were killed by decapitation, and gastric emptying was estimated at 10 and 30 min after ingestion. The effects of the sulfated form of CCK-8 (CCK-8S) and of graded doses of atropine were examined. In addition, a proton pump inhibitor was administered to wild-type mice to examine the contribution of gastric acid to emptying.ResultsGastric 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.ConclusionsThe gastric emptying of a nonnutrient liquid load was enhanced in mice without CCK-BR, although the precise mechanism is not known.