Area of Regulatory Biology, Division of Life Science, Graduate School of Science and Engineering, Saitama University, 255 Shimo-ohkubo, Sakuraku, Saitama 338-8570, Japan.
Area of Regulatory Biology, Division of Life Science, Graduate School of Science and Engineering, Saitama University, 255 Shimo-ohkubo, Sakuraku, Saitama 338-8570, Japan; Research Area of Evolutionary Molecular Design, Graduate School of Science and Engineering, Saitama University, 255 Shimo-ohkubo, Sakuraku, Saitama 338-8570, Japan.
Gen Comp Endocrinol. 2023 Oct 1;342:114352. doi: 10.1016/j.ygcen.2023.114352. Epub 2023 Jul 29.
In a fasting gastrointestinal tract, a characteristic cyclical rhythmic migrating motor complex (MMC) occur that comprises of three phases: I, II, and III. Among these, phase III contractions propagate from the stomach to the lower intestine in mammals, including humans, dogs, and Suncus murinus (suncus). Apart from the phase III of MMC propagating from the stomach, during the gastric phase II, small intestine-originated strong contractions propagate to the lower small intestine; however, the mechanism of contractions originating in the small intestine has not been clarified. In this study, we aimed to elucidate the role of cholecystokinin (CCK) in small intestinal motility. Administration of sulfated CCK-8 in phase I induced phase II-like contractions in the small intestine, which lasted for approximately 10-20 min and then returned to the baseline, while no change was observed in the stomach. Contractions of small intestine induced by CCK-8 were abolished by lorglumide, a CCK1 receptor antagonist. Gastrin, a ligand for the CCK2 receptor, evoked strong contractions in the stomach, but did not induce contractions in the small intestine. To examine the effect of endogenous CCK on contractions of small intestinal origin, lorglumide was administered during phase II. However, there was no change in the duodenal motility pattern, and strong contractions of small intestinal origin were not abolished by treatment with lorglumide. These results suggest that exogenous CCK stimulates contractions of small intestine via CCK1 receptors, whereas endogenous CCK is not involved in the strong contractions of small intestinal origin.
在禁食的胃肠道中，会出现一种特征性的周期性移行性运动复合波（MMC），它由三个阶段组成：I 期、II 期和 III 期。在这些阶段中，III 期收缩在哺乳动物（包括人类、狗和沙鼠）中从胃传播到下消化道。除了 MMC 的 III 期从胃传播外，在胃 II 期期间，起源于小肠的强烈收缩传播到下小肠；然而，起源于小肠的收缩机制尚未阐明。在这项研究中，我们旨在阐明胆囊收缩素（CCK）在小肠运动中的作用。在 I 期给予硫酸化 CCK-8 可诱导小肠出现类似 II 期的收缩，持续约 10-20 分钟，然后恢复基线，而胃无变化。CCK-8 诱导的小肠收缩被 CCK1 受体拮抗剂 lorglumide 消除。胃泌素是 CCK2 受体的配体，它在胃中引起强烈的收缩，但不会引起小肠收缩。为了研究内源性 CCK 对起源于小肠的收缩的影响，在 II 期给予 lorglumide。然而，十二指肠运动模式没有变化，并且 lorglumide 处理并没有消除起源于小肠的强烈收缩。这些结果表明，外源性 CCK 通过 CCK1 受体刺激小肠收缩，而内源性 CCK 不参与起源于小肠的强烈收缩。
