The study for functional correlation between palatability and gastric motility induced by appetite-enhancing peptides.

本研究探讨了食欲增强肽诱导胃运动与适口性之间的功能相关性。本实验观察了神经肽Y(NPY)对麻醉大鼠近端胃运动的影响。第四脑室注射NPY可引起近端胃的松弛，并呈剂量依赖性。给予Y1受体激动剂(Y1R)可有效地引起松弛，而不是NPY。迷走神经背侧复合体尾侧区(c-DVC)微量注射Y1R激动剂可引起近端胃的松弛。在双侧c-DVC注射Y1R拮抗剂后，第四脑室注射NPY不能引起松弛。这些结果表明，NPY通过位于DVC的Y1R引起近端胃的松弛。同时观察了Ghrelin对近端胃运动的影响。第四脑室注射Ghrelin诱发松弛…近端胃离子增多，呈剂量依赖关系。同时给予Ghrelin和GHS-R拮抗剂对IGP无明显影响。C-DVC内微量注射Ghrelin可引起近端胃的松弛。这些结果表明，Ghrelin通过位于DVC的GHS-R和NPY引起近端胃的松弛。这些结果有力地表明，食欲增强肽促进胃的储藏功能，以适应身体对食欲增强神经肽引起的过度消费。然而，服用其他促进食欲的多肽，黑色素浓缩激素(MCH)，并没有引起胃部反应。脑室注射增食欲素、MCH和NPY可增加糖精摄取。饮用糖精后，食欲素和神经肽Y的信使核糖核酸水平升高，但不影响MCH。阿片类拮抗剂纳洛酮的预治疗可阻断食欲素和神经肽Y的促食欲作用。这些结果表明，甜味和可口口味促进的过度消费归因于食欲素和神经肽Y等促食欲素神经肽的激活，以及下游阿片系统的激活和消化功能的增强。较少

The functional correlation between palatability and gastric motility induced by appetite-enhancing peptides were investigated in this study. The effects of neuropeptide Y (NPY) on motility of the proximal stomach were examined in anaesthetized rats. The administration of NPY into the 4th ventricle induced relaxation of the proximal stomach in a dose-dependent manner. The administrations of Y1 receptor (Y1R) agonist induced relaxation potently rather than those of NPY. The microinjections of Y1R agonist into the caudal part of the dorsal vagal complex (c-DVC) induced relaxation of the proximal stomach. The administration of NPY into the 4th ventricle did not induce relaxation after bilateral injection of Y1R antagonist into the c-DVC. These results revealed that NPY induced the relaxation in the proximal stomach via Y1R situated in the DVC. The effect of ghrelin on motility of the proximal stomach was also examined. The administration of ghrelin into the fourth ventricle induced relaxat … More ion of the proximal stomach in a dose-dependent manner. Simultaneous administration of ghrelin and GHS-R antagonist did not induce significant change in IGP. Microinjections of ghrelin into the c-DVC induced relaxation of the proximal stomach. These results indicate that ghrelin induces the relaxation of the proximal stomach via the GHS-R situated in the DVC as well as NPY. These results strongly suggest that the appetite-enhancing peptide facilitate reservoir function of the stomach to accommodate body to overconsumption elicited by the appetite-enhancing neuropeptides. However, the administration of the other appetite-enhancing peptides, melanin-concentrating hormone (MCH), did not induce gastric response. Intracerebroventricular (ICV) administrations of orexin, MCH and NPY increased the intake of saccharin. Drinking of saccharin in turn elevated the mRNA levels of orexin and NPY, but not MCH. Pre-treatments of naloxone, an opioid antagonist, blocked the orexigenic effects of orexin and NPY. These results suggest that the overconsumption promoted by sweet and palatable tastes is attributed to the activation of orexigenic neuropeptides, such as orexin and NPY, and a downstream opioid system together with enhanced digestive functions. Less