Washington Martha C, Williams Kasey, Sayegh Ayman I
Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088, United States.
Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088, United States.
Horm Behav. 2016 Feb;78:79-85. doi: 10.1016/j.yhbeh.2015.10.019. Epub 2015 Oct 30.
The current study tested the hypothesis that cholecystokinin (CCK) A receptor (CCKAR) in areas supplied by the celiac artery (CA), stomach and upper duodenum, and the cranial mesenteric artery (CMA), small and parts of the large intestine, is necessary for reduction of meal size, prolongation of the intermeal interval (time between first and second meal) and increased satiety ratio (intermeal interval/meal size or amount of food consumed during any given unit of time) by the non-nutrient stimulator of endogenous CCK release camostat. Consistent with our previous findings camostat reduced meal size, prolonged the intermeal interval and increased the satiety ratio. Here, we report that blocking CCKAR in the area supplied by the celiac artery attenuated reduction of meal size by camostat more so than the cranial mesenteric artery route. Blocking CCKAR in the area supplied by the cranial mesenteric artery attenuated prolongation of the intermeal interval length and increased satiety ratio by camostat more so than the celiac artery route. Blocking CCKAR in the areas supplied by the femoral artery (control) failed to alter the feeding responses evoked by camostat. These results support the hypothesis that CCKAR in the area supplied by the CA is necessary for reduction of meal size by camostat whereas CCKAR in the area supplied by the CMA is necessary for prolongation of the intermeal interval and increased satiety ratio by this substance. Our results demonstrate that meal size and intermeal interval length by camostat are regulated through different gastrointestinal sites.
在内脏动脉(CA)、胃和十二指肠上部所供应区域,以及肠系膜上动脉(CMA)、小肠和部分大肠中,胆囊收缩素(CCK)A受体(CCKAR)对于内源性CCK释放刺激剂抑肽酶减少进餐量、延长进餐间隔时间(第一餐和第二餐之间的时间)以及提高饱腹感比值(进餐间隔时间/进餐量或在任何给定单位时间内消耗的食物量)是必需的。与我们之前的研究结果一致,抑肽酶减少了进餐量,延长了进餐间隔时间,并提高了饱腹感比值。在此,我们报告,在内脏动脉所供应区域阻断CCKAR,与通过肠系膜上动脉途径相比,抑肽酶对进餐量减少的作用减弱得更明显。在肠系膜上动脉所供应区域阻断CCKAR,与通过内脏动脉途径相比,抑肽酶对进餐间隔时间延长和饱腹感比值提高的作用减弱得更明显。在股动脉(对照)所供应区域阻断CCKAR未能改变抑肽酶引起的进食反应。这些结果支持了以下假设:在内脏动脉所供应区域的CCKAR对于抑肽酶减少进餐量是必需的,而在肠系膜上动脉所供应区域的CCKAR对于该物质延长进餐间隔时间和提高饱腹感比值是必需的。我们的结果表明,抑肽酶对进餐量和进餐间隔时间的调节是通过不同的胃肠道部位实现的。