卸载诱导的骨间接接会改变下丘脑信号,促进骨质损失和脂肪代谢
Qiaoyue Guo1,2, Ningrong Chen1, Kalp Patel1
1Department of Orthopedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
|October 26, 2023
概括
太空飞行通过改变大脑信号导致骨质损失. 减少的前列腺素E2 (PGE2) 在下丘脑中触发神经Y (NPY) 和氨酸氧酶 (TH),影响骨和新陈代谢.
科学领域:
- 神经科学是一个神经科学.
- 骨生物学 骨生物学
- 空间生理学 空间生理学
背景情况:
- 微重力显著影响人类生理学,特别是在太空飞行期间引起骨质损失和中枢神经系统障碍.
- 正确的细胞和分子机制背后的这些生理变化响应微重力仍然在很大程度上是未知的.
- 骨整体感受,神经系统对身体内部状态的感知,与这些微重力诱导的效应有关.
研究的目的:
- 阐明分子机制,将微重力诱导的卸载与骨质损失和改变的新陈代谢联系起来.
- 为了研究下丘脑神经Y (NPY) 和氨酸氧酶 (TH) 在调解这些效应中的作用.
- 探索骨互感,中央神经内分泌信号和交感神经系统活动之间的相互作用.
主要方法:
- 利用小鼠后肢卸载模型来模拟微重力条件.
- 在下丘脑中测量了神经Y (NPY) 和氨酸氧酶 (TH) 的表达水平.
- 使用了交感性抗剂 (propranolol),基因修饰 (骨细胞中的Adrb2删除),以及针对诺拉上腺素和NPY的药理干预措施.
主要成果:
- 后肢卸载增加了下丘脑NPY和TH表达,导致骨质损失和脂肪代谢的改变.
- 减少的前列腺素E2 (PGE2) 介导的受体信号传递在增强的下丘脑TH和NPY表达之前.
- 交感阻塞 (propranolol),骨细胞中的Adrb2删除和抑制北上腺素释放改善了骨损失;NPY抑制主要影响食物摄入和能量消耗.
结论:
- 减少PGE2介导的骨内感受信号是下载期间中枢神经系统和骨变化的关键发起者.
- 低垂体NPY通过交感TH活动促进骨形成,突出显示神经内分泌-骨轴.
- 这些发现揭示了骨和中枢神经系统之间相互调节的途径,以应对微重力诱导的卸载.
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