LOUISIANA COBRE: P4: MECHANISMS OF AGING-INDUCED LEPTIN RESISTANCE AND OBESITY

路易斯安那 COBRE：P4：衰老引起的瘦素抵抗和肥胖的机制

• 批准号: 8167952
• 负责人: Christopher D Morrison
• 金额: $ 20.58万
• 依托单位: LSU PENNINGTON BIOMEDICAL RESEARCH CTR
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-07-01 至 2011-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8167952
• 关键词: Age; Aging; Animals; Antioxidants; Area; Behavior; Brain; Computer Retrieval of Information on Scientific Projects Database; Diet; Fatty acid glycerol esters; Funding; Grant; Hippocampus (Brain); Hypothalamic structure; Institution; Leptin; Leptin resistance; Louisiana; Metabolism; Neurons; Obesity; Oxidative Stress; Research; Research Personnel; Resources; Signal Transduction; Source; Testing; United States National Institutes of Health; enzyme activity

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. A. Specific Aims Specific Aim 1: Test the hypothesis that aging enhances the negative effects of high fat diet (HFD) on brain leptin signaling, metabolism and behavior. Specific Aim 2: Test the hypothesis that aging will impair the ability of the animal to reduce body adiposity and recover normal brain leptin signaling following cessation of a HFD. Specific Aim 3: Test the hypothesis that leptin protects against oxidative stress in hypothalamic and hippocampal neurons by enhancing antioxidant enzyme activity via NRF2 signaling. Specific Aim 4: Determine the functional interaction between leptin signaling and oxidative stress within areas of the hippocampus and hypothalamus.

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。 A. 具体目标 具体目标 1：检验以下假设：衰老会增强高脂肪饮食 (HFD) 对大脑瘦素信号、代谢和行为的负面影响。 具体目标 2：检验以下假设：衰老会损害动物在停止 HFD 后减少身体肥胖和恢复正常大脑瘦素信号传导的能力。 具体目标 3：检验瘦素通过 NRF2 信号传导增强抗氧化酶活性来保护下丘脑和海马神经元免受氧化应激的假设。 具体目标 4：确定海马和下丘脑区域内瘦素信号传导与氧化应激之间的功能相互作用。