CENTRAL REGULATION OF SYMPATHETIC ACTIVITY TO BROWN FAT

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 平衡能量消耗与能量摄入、代谢需求和能量储存对于保持体重、对葡萄糖、胰岛素和瘦素等代谢信号的持续反应以及对许多身体系统的动态平衡调节至关重要。我们的实验正在定义和检验这样一个假设，即蝙蝠的能量消耗是消耗多余能量摄入的潜在汇，以防止白色脂肪组织中过度储存能量。明确能量传入信号通路，以及控制蝙蝠能量消耗效应的传出神经通路，将有助于我们理解体重和能量底物可用性的调节，并有助于设计治疗策略，以控制导致肥胖、糖尿病和高血压等疾病的身体能量平衡失调。最近的发现包括从视前区到下丘脑背内侧和中缝苍白球的不同投射的识别，下丘脑室旁神经元对BAT的抑制影响的特征，以及脊髓5-羟色胺释放在降温引起的BAT产热和能量消耗增加中的重要作用。

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.