交感性神经Y通过维持发热脂肪来防止肥胖
Yitao Zhu1, Lu Yao1, Ana L Gallo-Ferraz2
1Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Nature
|August 28, 2024
概括
来自交感神经的神经Y (NPY) 通过维持能量消耗来预防肥胖. 这些神经元中的NPY损失会导致肥胖,并降低身体燃烧卡路里的能力.
科学领域:
- 神经内分泌学
- 代谢调节
- 脂肪组织生物学
背景情况:
- 人类神经Y (NPY) 突变与高体重指数相关.
- 关于肥胖的同情神经元中NPY的确切作用尚不清楚.
- 脂肪组织,包括棕色 (BAT) 和白色 (WAT),在能量平衡中起着至关重要的作用.
研究的目的:
- 阐明同情神经元中NPY保护肥胖的机制.
- 研究NPY,脂肪组织和能量消耗之间的相互作用.
- 确定NPY缺乏对交感神经元对代谢健康的影响.
主要方法:
- 在被清除的小鼠脂肪组织 (BAT和WAT) 上使用先进的成像技术.
- 分析单细胞RNA测序数据集以识别NPY响应细胞.
- 在交感神经元中生成并研究NPY的小鼠模型.
主要成果:
- 表达NPY的交感轴突主要与脂肪组织中的周血管有关.
- 墙体细胞被确定为主要的NPY反应细胞,对热生成脂肪细胞产生至关重要.
- 饮食诱导的肥胖导致NPY+轴突的神经病变和壁细胞的枯竭.
- 同情性NPY的损失导致白色的BAT,降低了热生成,减少了能量消耗,导致肥胖.
- 缺乏同情性NPY的小鼠在没有改变食物摄入的情况下发展成成人肥胖症和增加对饮食诱导的肥胖症的敏感性.
结论:
- 来自交感神经的外围NPY维持能量消耗,反对中央NPY对体重的影响.
- 脂肪组织壁细胞中的NPY信号对于维持发热能力和预防肥胖至关重要.
- 交感性NPY缺乏会破坏能量平衡,突出显示它在代谢调节中的关键作用,独立于食物摄入.
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