Obesity Laboratory, Instituto Gulbenkian de Ciência, Oeiras 2780-156, Portugal.
Obesity Laboratory, Instituto Gulbenkian de Ciência, Oeiras 2780-156, Portugal; The Howard Hughes Medical Institute (HHMI) International Research Scholars Program, Portugal; Department of Physiology, Anatomy, and Genetics, University of Oxford, OX1 3PT, UK.
Cell Immunol. 2018 Aug;330:183-187. doi: 10.1016/j.cellimm.2018.04.014. Epub 2018 May 3.
Obesity is a worldwide public health concern yet no safe therapies are currently available. The activity of sympathetic neurons is necessary and sufficient for fat mass reduction, via norepinephrine (NE) signaling. Macrophage accumulation in the adipose tissue is thought to play the central role in the onset of obesity, yet their relation to NE has been controversial. We have identified a population of sympathetic neuron-associated macrophages (SAMs) that control obesity via the uptake and clearing of NE. Here we focus on the neuro-immune regulation of obesity by discussing the genetic, cellular and functional signatures of SAMs vis-a-vis adipose tissue macrophages (ATMs).
肥胖是一个全球性的公共健康问题,但目前尚无安全有效的治疗方法。通过去甲肾上腺素(NE)信号,交感神经元的活动对于减少脂肪量是必要且充分的。脂肪组织中巨噬细胞的积累被认为在肥胖的发生中起着核心作用,但它们与 NE 的关系一直存在争议。我们已经鉴定出一群与交感神经元相关的巨噬细胞(SAMs),它们通过摄取和清除 NE 来控制肥胖。在这里,我们通过讨论 SAM 相对于脂肪组织巨噬细胞(ATMs)的遗传、细胞和功能特征,来关注神经免疫对肥胖的调节。