UPPER GI TRACT MEDIATION OF THE SATIETY EFFECT OF FATS

上消化道对脂肪饱腹感的调节

• 批准号: 3462816
• 负责人: DANIELLE GREENBERG
• 金额: $ 8.54万
• 依托单位: WEILL MEDICAL COLL OF CORNELL UNIV
• 依托单位国家: 美国
• 财政年份: 1988
• 资助国家: 美国
• 起止时间: 1988-04-01 至 1993-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3462816
• 关键词: dietary lipid; gastrointestinal system; hormone regulation /control mechanism; hunger; laboratory rat; neural information processing; neuroendocrine system; nutrition related tag; satiations; sham feeding

The physiological mechanism by which ingested fats terminate eating in animals and humans is unknown. This proposal is designed: (1) to elucidate the critical stimuli for fat-induced postprandial satiety; (2) to determine the site of action for such stimuli; and (3) to examine the neural, endocrine or neuroendocrine mechanisms involved in mediating this satiety response in Sprague Dawley rats. Knowlege of such mechanisms are likely to be of major importance for developing effective treatments for the control of eating disorders, such as obesity and bulimia. There is evidence that genetically obese animals and humans are less responsive to the satiating effects of fats. Therefore, a secondary aim of this proposal is to examine differences in fat-induced satiety between lean and genetically obese rats. To determine the critical stimuli involved in fat-induced satiety, tests will be carried out with specific short-, medium-, long-, and very long-chain fats. These substances will be assayed for their effects on satiety by infusing them directly into stomach or duodenum of rats feeding normally or sham feeding. The site of action for inducing satiety will be determined by measuring triglyceride levels in the blood subsequent to infusions, infusing fats into the hepatic-portal vein or the inferior vena cava, on confing fats in the stomach, of sham and real feeding rats. Experiments to determine the neural and/or hormal mechanisms that mediate those fat stimuli determined to be most effective for inducing satiety are also proposed. Total subdiaphragmatic vagotomy, selective vagotomies, selective afferent and efferent vagotomy and spinal visceral disconnection will be used to analyze neural mechanisms mediating fat-induced satiety. Measurement of peptides and the use of selective peptide antagonists will be used to assess the involvement of intestinal hormones in mediating the satiating response to those fats that are the most potent stimuli for inducing satiety. The specificity of fats for inhibition of various oral stimuli will be assessed. Those fat stimuli that are most effective for inducing satiety and those mechanisms that are found to mediate the satiety response in Sprague Dawley rats will be subsequently tested in identical paradigms in lean and obese Zucker rats.

终止摄入脂肪的生理机制 动物和人类的食用情况尚不清楚。 这个提议是 设计：（1）阐明脂肪诱导的关键刺激 餐后饱腹感； (2) 确定此类行为的作用地点 刺激； (3) 检查神经、内分泌或 参与调节这种饱腹感的神经内分泌机制 斯普拉格道利大鼠的反应。 了解此类机制 可能对于开发有效的 控制饮食失调的治疗，例如肥胖和 暴食症。 有证据表明，遗传性肥胖的动物和 人类对脂肪的饱足感反应较弱。 因此，本提案的第二个目标是审查 瘦肉和遗传脂肪引起的饱腹感存在差异 肥胖的老鼠。 为了确定脂肪引起的饱腹感所涉及的关键刺激， 测试将以特定的短、中、长和 非常长链的脂肪。 这些物质将被检测其 将它们直接注入胃中或对饱腹感产生影响 正常喂养或假喂养的大鼠十二指肠。 该网站的 引起饱腹感的作用将通过测量来确定 输注后血液中的甘油三酯水平 脂肪进入肝门静脉或下腔静脉 假鼠和真鼠的胃中混有脂肪。 确定神经和/或激素机制的实验 介导那些被认为是最有效的脂肪刺激 还提出了诱导饱腹感的方法。 全膈下 迷走神经切断术、选择性迷走神经切断术、选择性传入和传出神经切断术 迷走神经切断术和脊柱内脏断开术将用于分析 介导脂肪引起的饱腹感的神经机制。 测量 肽和选择性肽拮抗剂的使用将是 用于评估肠道激素的参与 调节对那些最重要的脂肪的饱足反应 产生饱腹感的有效刺激。 脂肪的特殊性 将评估各种口腔刺激的抑制。 那些最能有效引起饱腹感的脂肪刺激物 那些被发现介导饱腹感反应的机制 随后将在斯普拉格道利大鼠中进行相同的测试 瘦和肥胖 Zucker 大鼠的范例。