神经介质单元通过大脑脂肪回路控制ILC2和肥胖
Filipa Cardoso1,2, Roel G J Klein Wolterink1, Cristina Godinho-Silva1
1Champalimaud Research, Champalimaud Centre for the Unknown, Lisbon, Portugal.
Nature
|August 19, 2021
概括
一个涉及同情神经和介质细胞的新型大脑脂肪循环控制脂肪中的免疫细胞. 这种神经介质单元通过调节2组先天性淋巴细胞 (ILC2) 来影响新陈代谢,胰岛素抵抗和肥胖.
科学领域:
- 神经内分泌学
- 免疫学
- 代谢研究
背景情况:
- 神经和免疫系统的相互作用是炎症和宿主防御的关键调节者.
- 神经免疫合作在通过大脑与身体轴调节新陈代谢和肥胖的作用尚不清楚.
- 脂肪组织生物学受到同情神经元和免疫细胞的信号的影响.
研究的目的:
- 研究神经元和免疫细胞在调节新陈代谢和肥胖方面的合作.
- 通过脑脂肪电路识别控制脂肪组织生理,新陈代谢和肥胖的神经介质单元.
主要方法:
- 分析了交感神经末端活动及其对脂肪介质细胞的影响.
- 评估了质衍生神经营养因子 (GDNF) 表达和2组先天性淋巴细胞 (ILC2) 活性.
- 通过逆行追踪,化学,手术和化学遗传学操作来绘制神经回路.
主要成果:
- 交感神经终端通过β2上腺体受体调节脂肪介质细胞,控制阴道脂肪中的GDNF表达和ILC2活性.
- 对GDNF受体路径的ILC2特异性操纵改变了ILC2功能,能量消耗,胰岛素耐药性和肥胖易感性.
- 鉴定出一个连接淋巴体脂肪ILC2s与下丘脑区域的交感大动脉回路.
结论:
- 一个神经介质单元将神经元信号转化为脂肪内存在的ILC2功能,影响宿主代谢和肥胖.
- 这种大脑脂肪循环突显出一种调节能量平衡和新陈代谢健康的新机制.
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