Cholecystokinin (CCK) had been the first gastrointestinal hormone known to exert anorexic effects. CCK had been inferred to contribute to the onset of functional dyspepsia (FD) symptoms. To understand the pathophysiology of FD, the roles of stress have to be clarified. In this study, we aimed to clarify the influence of stress on the action of cholecystokinin (CCK) on appetite and gastric emptying. Using rats, stress was simulated by giving restraint stress or intraperitoneal injection of the stress-related peptide hormone urocortin 1 (UCN1). The effects of CCK and restraint stress, alone or in combination, on food intake and gastric motility were examined, and c-Fos expression in the neurons of appetite control network in the central nervous system was assessed by immunohistochemical staining. CCK inhibited food intake and gastric emptying in a dose-dependent manner. Food intake for 1 h was significantly lower with UCN1 (2 nmol/kg) than with the saline control. Restraint stress amplified the suppressive effects of CCK on food intake for 1 h and on gastric emptying. With regard to brain function, the CCK induced c-Fos expression in the neurons of the nucleus tractus solitarius and paraventricular nucleus of the hypothalamus was markedly and significantly amplified by the addition of restraint stress with CCK. The results suggested that stress might amplify the anorexic effects of CCK through activation of the nuclei that comprise the brain neuronal network for satiation; this might play a role in the pathogenesis of the postprandial distress syndromes of functional dyspepsia.

胆囊收缩素（CCK）是已知的第一种具有厌食作用的胃肠激素。推测CCK可导致功能性消化不良（FD）症状的发作。要了解FD的病理生理学，必须明确压力的作用。在这项研究中，我们旨在阐明压力对胆囊收缩素（CCK）对食欲和胃排空的作用的影响。通过使用大鼠，通过束缚压力或腹膜内注射与压力有关的肽激素urocortin 1（UCN1）来模拟压力。检查了CCK和束缚应激单独或组合对食物摄入和胃蠕动的影响，并通过免疫组织化学染色评估了中枢神经系统食欲控制网络神经元中c-Fos的表达。CCK以剂量依赖性方式抑制食物摄入和胃排空。使用UCN1（2 nmol / kg）1小时的食物摄入量显着低于盐水对照组。约束压力放大了CCK对食物摄入1 h和胃排空的抑制作用。关于脑功能，CCK诱导的下丘脑孤束核和室旁核神经元中的c-Fos表达被CCK施加束缚应激而显着并显着放大。结果表明，应激可能会通过激活构成满足饱食状态的大脑神经元网络的核而增强CCK的厌食作用。这可能在功能性消化不良的餐后窘迫综合征的发病机理中起作用。使用UCN1（2 nmol / kg）1小时的食物摄入量显着低于盐水对照组。约束压力放大了CCK对食物摄入1 h和胃排空的抑制作用。关于脑功能，CCK诱导的下丘脑孤束核和室旁核神经元中的c-Fos表达被CCK施加束缚应激而显着并显着放大。结果表明，应激可能会通过激活构成满足饱食状态的大脑神经元网络的核而增强CCK的厌食作用。这可能在功能性消化不良的餐后窘迫综合征的发病机理中起作用。使用UCN1（2 nmol / kg）1小时的食物摄入量显着低于盐水对照组。约束压力放大了CCK对食物摄入1 h和胃排空的抑制作用。关于脑功能，CCK诱导的下丘脑孤束核和室旁核神经元中的c-Fos表达被CCK施加束缚应激而显着并显着放大。结果表明，压力可能会通过激活构成满足饱食状态的大脑神经元网络的细胞核而增强CCK的厌食作用。这可能在功能性消化不良的餐后窘迫综合征的发病机理中起作用。约束压力放大了CCK对食物摄入1 h和胃排空的抑制作用。关于脑功能，CCK诱导的下丘脑孤束核和室旁核神经元中的c-Fos表达被CCK施加束缚应激而显着并显着放大。结果表明，压力可能会通过激活构成满足饱食状态的大脑神经元网络的细胞核而增强CCK的厌食作用。这可能在功能性消化不良的餐后窘迫综合征的发病机理中起作用。约束压力放大了CCK对食物摄入1 h和胃排空的抑制作用。关于脑功能，CCK诱导的下丘脑孤束核和室旁核神经元中的c-Fos表达被CCK施加束缚应激而显着并显着放大。结果表明，应激可能会通过激活构成满足饱食状态的大脑神经元网络的核而增强CCK的厌食作用。这可能在功能性消化不良的餐后窘迫综合征的发病机理中起作用。CCK诱导的束缚应激增加了CCK诱导的下丘脑孤束核和室旁核神经元中c-Fos表达。结果表明，应激可能会通过激活构成满足饱食状态的大脑神经元网络的核而增强CCK的厌食作用。这可能在功能性消化不良的餐后窘迫综合征的发病机理中起作用。CCK诱导的束缚应激增加了CCK诱导的下丘脑孤束核和室旁核神经元中c-Fos表达。结果表明，压力可能会通过激活构成满足饱食状态的大脑神经元网络的细胞核而增强CCK的厌食作用。这可能在功能性消化不良的餐后窘迫综合征的发病机理中起作用。