REGULATION OF FOOD INTAKE--BRAIN AND GUT MEDIATORS

食物摄入的调节——大脑和肠道介质

• 批准号: 3463668
• 负责人: THEODORE PAPPAS
• 金额: $ 9.17万
• 依托单位: DUKE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1988
• 资助国家: 美国
• 起止时间: 1988-12-01 至 1993-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3463668
• 关键词: appetite regulatory center; autonomic nervous system; biological models; cholecystokinin; diet route /schedule; dogs; eating; efferent nerve; gastrointestinal nutrient absorption; hypothalamus; neuropeptides; nutrition related tag; sham feeding; stomach emptying

Regulatory signals from the brain and gut control appetite. Two neuropeptides thought to have a primary role in the hypothalamic feeding centers are neuropeptide Y (NPY), an orexigenic, and cholecystokinin (CCK) a satiety factor. Gut signals appear to act through hypothalamic brain peptides to regulate feeding. Signals sent to the hypothalamus during gastric distension, intestinal passage of nutrients, and postabsorptive sensation of caloric intake, may influence satiety. Unfortunately, the current body of information is not adequate for a full understanding of the neuropeptidergic control of the satiety cascade. Our preliminary experiments in a canine feeding model have begun to clarify some of these central and peripheral satiety signals. This model of cerebroventricular cannulation and true sham feeding in the dog is the basis for the studies detailed in the following seven specific aims: 1. Characterize the central and peripheral effects of NPY on sham feeding and determine whether central NPY is a physiologic stimulator of feeding in the dog. 2. Determine if central NPY is the final event in the initiation of feeding by characterizing its effects against several known satiety signals (i.e., gastric distension, intestinal and intravenous nutrients, central CCK and naloxone). 3. Characterize central CCK's satiety inducing effect against a variety of feeding signals (i.e., starvation, central endorphine and NPY and highly palatable food). 4. Determine whether there is a relationship between the central effect of CCK/NPY on feeding and gastric emptying. 5. Determine whether gastric distension-induced satiety is mediated by the central release of CCK, and if that release is vagal mediated. 6. Determine the effect of intestinal perfusion (jejunal, ileal or colonic) with nutrients (fats, carbohydrates, proteins) on sham feeding. 7. Study the effect of chronic intravenous feeding (fats, carbohydrates, proteins or mixed) versus enteral feeding on sham feeding. From these studies we hope to better understand the relative importance of a variety of signals and eventually construct an integrated satiety cascade. This information is a necessary prerequisite to our understanding of disease processes associated with disturbances in nutrient intake, such as anorexia nervosa and bulemia.

来自大脑和肠道控制食欲的调节信号。 二 神经肽被认为在下丘脑进食中起主要作用 中心是神经肽Y（NPY），一种甲状腺素和胆囊动蛋白 （CCK）一个饱腹感因素。 肠道信号似乎通过下丘脑起作用 脑肽调节进食。 发送给下丘脑的信号 在胃扩张期间，营养素的肠道通过和 热量摄入量的吸收后感觉可能会影响饱腹感。 不幸的是，目前的信息体系不足以满足 了解饱腹级别的神经肽控制。 我们在犬喂养模型中的初步实验已经开始 澄清其中一些中心和外围饱腹感信号。 这个模型 在狗中脑室插管和真正的假喂食是 在以下七个特定目标中详细介绍的研究的基础：1。 表征NPY对假喂养的中心和外围影响 并确定Central NPY是否是进食的生理刺激剂 在狗中。 2。确定中央npy是否是最终事件 通过表征其对几个已知的效果来启动进食 饱腹感信号（即胃扩张，肠道和静脉注射 营养，中央CCK和纳洛酮）。 3。表征中央CCK的 针对各种喂养信号的饱腹感（即 饥饿，中孔和NPY和高度可口的食物）。 4。 确定中心效应之间是否存在关系 cck/npy喂食和胃排空。 5。确定是否胃 延伸引起的饱腹感由CCK的中央释放介导，并且 如果该版本是迷走神经介导的。 6。确定肠的影响 灌注（空肠，卵形或结肠），含有营养（脂肪， 碳水化合物，蛋白质）假喂食。 7。研究慢性的效果 静脉注射（脂肪，碳水化合物，蛋白质或混合）与 肠内喂食。 从这些研究中，我们希望更好地了解相对重要性 各种信号，最终建造一个综合的饱腹感 级联。 这些信息是我们的必要先决条件 了解与疾病相关的疾病过程 营养摄入量，例如神经性厌食症和泡沫症。