CENTRAL REGULATION OF SYMPATHETIC ACTIVITY TO BROWN FAT

棕色脂肪交感神经活动的中枢调节

• 批准号: 8173282
• 负责人: SHAUN F MORRISON
• 金额: $ 12.37万
• 依托单位: OREGON HEALTH & SCIENCE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8173282
• 关键词: Adipose tissue; Body Weight; Brown Fat; Computer Retrieval of Information on Scientific Projects Database; Consumption; Diabetes Mellitus; Disease; Energy Intake; Energy Metabolism; Equilibrium; Funding; Glucose; Grant; Homeostasis; Hypertension; Hypothalamic structure; Institution; Insulin; Leptin; Maintenance; Metabolic; Neural Pathways; Neurons; Obesity; Preoptic Areas; Regulation; Research; Research Personnel; Resources; Role; Serotonin; Signal Pathway; Signal Transduction; Source; Spinal; Testing; Therapeutic; Thermogenesis; United States National Institutes of Health; body system; design; prevent; research study

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. Balancing energy expenditure with energy intake, metabolic requirements and energy storage is critical for maintenance of body weight, for sustained responsiveness to metabolic signals such as glucose, insulin and leptin and for homeostatic regulation of many body systems. Our experiments are defining and testing the hypothesis that energy expenditure in BAT is a potential sink for the consumption of surplus energy intake to prevent excess energy storage in white adipose tissue. Defining energy afferent signaling pathways, as well as those efferent neural pathways controlling the BAT energy expenditure effector will contribute to our understanding of the regulation of body weight and of energy substrate availability and to the design of therapeutic strategies to control disturbances in body energy homeostasis that result in diseases such as obesity, diabetes and hypertension. Recent findings include the identification of distinct projections from the preoptic area to the dorsomedial hypothalamus and to the raphe pallidus, the characterization of an inhibitory influence on BAT from paraventricular hypothalamic neurons and the determination of a prominent role for spinal serotonin release in the cooling-evoked increase in BAT thermogenesis and energy expenditure.

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。子项目及 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。 平衡能量消耗与能量摄入、代谢需求和能量储存对于维持体重、对葡萄糖、胰岛素和瘦素等代谢信号的持续反应以及许多身体系统的稳态调节至关重要。我们的实验正在定义和测试这样的假设：BAT 中的能量消耗是消耗剩余能量摄入的潜在汇，以防止白色脂肪组织中储存过多的能量。定义能量传入信号通路以及控制 BAT 能量消耗效应器的传出神经通路将有助于我们了解体重调节和能量底物可用性，并有助于设计控制身体能量稳态紊乱的治疗策略。导致肥胖、糖尿病、高血压等疾病。 最近的发现包括识别从视前区到下丘脑背内侧和苍白中缝的不同投射，表征室旁下丘脑神经元对 BAT 的抑制影响，以及确定脊髓血清素释放在冷却诱发中的重要作用。 BAT 产热和能量消耗增加。