NEUROSCIENCE CENTER FOR INGESTIVE BEHAVIOR

摄取行为神经科学中心

• 批准号: 7562402
• 负责人: ROBERT E SHADE
• 金额: $ 12.01万
• 依托单位: TEXAS BIOMEDICAL RESEARCH INSTITUTE
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-05-01 至 2008-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7562402
• 关键词: Animals; Appetitive Behavior; Behavior; Blood Pressure; Computer Retrieval of Information on Scientific Projects Database; Desire for food; Disease; Elevation; Feeding behaviors; Funding; Future; Genetic; Grant; Homeostasis; Hormonal; Human; Institution; Kidney; Lead; Modeling; Neurosciences; Pan Genus; Pan troglodytes; Papio; Physiological; Primates; Research; Research Personnel; Resources; Risk Factors; Sodium Chloride; Sodium-Restricted Diet; Source; United States National Institutes of Health; Water; Water consumption; mouse model; programs; receptor; salt intake

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Ingestive behavior is a major factor in predisposing to a variety of diseases, but the neurohumoral mechanisms responsible for ingestive behavior are not well understood. An understanding of those mechanisms may lead to new strategies for controlling ingestive behaviors that are risk factors for specific diseases. This is a five component multi-investigator program that involves several institutions. The objectives are to develop a better understanding of the following 1. Neurohumoral organization of ingestive behavior in a mouse model. 2. Salt-sensitivity of blood pressure in a chimpanzee model. 3. Appetite mechanisms in humans and in a baboon model. 4. Neurohumoral control of salt and water intake in a baboon model. 5. Bran receptor mechanisms in a baboon model. Projects 2 and 4 are conducted at the SRPRC. The preliminary results for Project 2 support the hypothesis that an increase in dietary salt causes a significant elevation of blood pressure within 9 months, and the effect is reversible when the animals are returned to a low salt diet. Preliminary results for Project 4 support the hypothesis that hormonal factors related to renal salt and water homeostasis are important in regulating salt intake behavior in primates. It is expected that the results will provide sufficient date to enable future research on the physiological mechanisms that control salt appetite and the underlying genetic factors that control these mechanisms.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 摄食行为是诱发多种疾病的主要因素，但引起摄食行为的神经体液机制尚不清楚。 了解这些机制可能会导致控制作为特定疾病危险因素的摄入行为的新策略。 这是一个由五个组成部分的多研究者项目，涉及多个机构。 目的是更好地理解以下内容： 1. 小鼠模型中摄取行为的神经体液组织。 2. 黑猩猩模型中血压的盐敏感性。 3. 人类和狒狒模型的食欲机制。 4. 狒狒模型中盐和水摄入的神经体液控制。 5. 狒狒模型中的麸皮受体机制。 项目 2 和 4 在 SRPRC 进行。 项目 2 的初步结果支持这样的假设：膳食盐的增加会在 9 个月内导致血压显着升高，并且当动物恢复低盐饮食时，这种影响是可逆的。 项目 4 的初步结果支持这样的假设：与肾盐和水稳态相关的激素因素对于调节灵长类动物的盐摄入行为很重要。 预计这些结果将为未来研究控制盐食欲的生理机制以及控制这些机制的潜在遗传因素提供足够的数据。