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

本研究旨在探讨食欲增强肽对胃运动的影响及其与适口性的关系。本文观察了神经肽Y（NPY）对麻醉大鼠近端胃运动的影响。第四脑室注射神经肽Y可引起近端胃的舒张，并呈剂量依赖性。给予Y1受体激动剂比给予NPY更有效地引起舒张。在迷走神经背侧复合体（c-DVC）尾部微量注射Y1 R激动剂可引起近端胃的舒张。在双侧c-DVC注射Y1 R拮抗剂后，第四脑室注射NPY不引起舒张。结果表明，NPY通过位于DVC的Y1 R引起近端胃的舒张。还检查了ghrelin对近端胃运动的影响。第四脑室注射ghrelin可引起舒张反应， ...更多信息 离子的近端胃以剂量依赖性的方式。同时给予Ghrelin和GHS-R拮抗剂对IGP无明显影响。向c-DVC中微量注射ghrelin诱导近端胃的舒张。这些结果表明，ghrelin通过位于DVC的GHS-R以及NPY诱导近端胃的舒张。这些结果有力地表明，食欲增强肽促进胃的储库功能，以适应身体由食欲增强神经肽引起的过度消耗。然而，其他食欲增强肽，黑色素浓集激素（MCH）的管理，没有诱导胃反应。脑室内（ICV）给药食欲素，MCH和NPY增加糖精的摄入量。饮用糖精反过来会提高食欲素和NPY的mRNA水平，但不会提高MCH。阿片拮抗剂纳洛酮预处理可阻断食欲素和NPY的促食欲作用。这些结果表明，甜味和可口的味道促进的过度消费归因于食欲神经肽，如食欲素和NPY，以及下游阿片系统的激活，以及增强的消化功能。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