PEPTIDE YY--COLONIC GASTRIC AND PANCREATIC INHIBITION

肽YY（PYY）从远端肠道中的内分泌细胞释放， 对上消化道功能产生影响，即，抑制胰腺和 外分泌有证据表明，PYY可能是 “肠抑胃素”和“抗CCK”激素。PPY还可以 介导“回肠制动”现象，由此肠道运动减慢， 吸收不良的脸在本研究中，我们将扩展这些 通过1）对比不同管腔内 抑制酸分泌的营养素，其释放PYY的能力， 2)描述大肠和小肠的相对重要性 在这些现象中。其他研究将确定是否有一个作用， PYY在胰腺反馈控制中的作用。总的来说， 动物将通过在细胞水平上描绘来扩展， PYY的释放和作用机制。我们将研究 肾上腺素能激动剂和拮抗剂以及肽类激素 使用我们开发的分离培养的PYY细胞制备PYY。的 第二信使介导这些影响也将被描绘。 在 其他实验中，我们将对比结合和结构 肠PYY受体的特性与通用NPY-PYY 我们最近在大脑中分离并鉴定了这种受体。我们将 试图通过一系列步骤纯化受体， 亲和层析其他实验将确定 肠受体与中枢受体一样，通过 G蛋白对腺苷酸环化酶的抑制作用。最后，我们将测试 PYY中枢作用抑制胃迷走神经张力的假说。 我们推测，循环PYY暴露于一个亚群， 中枢NPY-PYY受体通过最后区后， 血脑屏障中已知存在渗漏的区域。这些研究 应该定义PYY的生理重要性，他们可以 描绘了这种肠道激素的独特机制和作用途径。

Peptide YY (PYY) is released from endocrine cells in the distal gut to exert effects on upper gut function i.e., to inhibit pancreatic and exocrine secretion. Evidence exists to show that PYY may be both the "enterogastrone" and "anti-CCK' hormone described by others. PPY may also mediate the "ileal brake" phenomenon whereby gut motility is slowed in the face of malabsorption. In the present study we will extend these observations by 1) contrasting the ability of different intraluminal nutrients to inhibit acid secretion with their ability to release PYY and 2) delineating the relative importance of the large and small intestine in these phenomena. Other studies will determine if there is a role for PYY in feedback control of the pancreas. These observations in the whole animal will be extended by delineating at the cellular level, the mechanisms of PYY's release and action. We will study the role of adrenergic agonists and antagonists and peptide hormones in the release of PYY using an isolated cultured PYY cell preparation we developed. The second messenger that mediates these effects will also be delineated. In other experiments we will contrast the binding and structural characteristics of the intestinal PYY receptor with the generic NPY-PYY receptor we recently isolated and characterized in the brain. We will attempt to purify the receptor in a series of steps culminating in affinity chromatography. Other experiments will determine if the intestinal receptor is, like the central receptor, linked through an inhibitory G protein to adenyl cyclase. Finally, we will test the hypothesis that PYY acts centrally to inhibit vagal tone on the stomach. We speculate that circulating PYY is exposed to a subpopulation of central NPY-PYY receptors after it passes through the Area Postrema, an area of the blood-brain barrier that is known to be leaky. These studies should define the physiologically importance of PYY and they may delineate a unique mechanism and route of action for this gut hormone.