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色脂肪细胞通过细胞外 inosine 增强能量消耗

Birte Niemann¹, Saskia Haufs-Brusberg², Laura Puetz²

¹Institute of Pharmacology and Toxicology, University Hospital, University of Bonn, Bonn, Germany. Bini@uni-bonn.de.

|July 5, 2022

概括

这是一种能增加能量消耗和抗肥胖的代谢物. 这一发现通过操纵素水平为代谢疾病提供了新的治疗点.

科学领域:

代谢研究
脂肪组织生物学
肥胖治疗方法

背景情况:

棕色脂肪组织 (BAT) 对于能量消耗和心脏代谢健康至关重要.
肥胖和老龄化导致BAT损失,阻碍肥胖治疗.
棕色脂肪细胞在新陈代谢调节中的作用尚不清楚.

研究的目的:

研究棕色脂肪细胞亡的代谢后果.
识别影响热生成的亡过程中释放的信号分子.
探索这些分子的治疗潜力以及它们对肥胖的途径.

主要方法:

不针对性代谢分析以分析色脂肪细胞分泌物.
在体外对健康脂肪细胞和人类棕色脂肪细胞的研究.
使用小鼠模型的体内研究 (药物抑制,基因切除).
人类脂肪组织和遗传变异的分析.

主要成果:

色脂肪细胞释放 purin 代谢物,特别是 inosine.
在棕色脂肪细胞中通过cAMP- PKA通路增强热生成基因表达和能量消耗.
在小鼠中,伊诺辛治疗增加了BAT活性,诱导了白色脂肪组织的色,并抵消了饮食引起的肥胖症.
平衡性核酸转运体1 (ENT1) 调节细胞外 inosine 水平;ENT1 抑制/缺陷增强了 BAT 活性和抗肥胖性.
在人类中,ENT1变体 (Ile216Thr) 与较低的BMI和降低的肥胖风险有关.

结论:

在亡过程中释放的"替代我"信号,调节热生成脂肪.
针对因诺辛-ENT1轴为肥胖症治疗提供了一种新的策略.
操纵素信号可以增加能量消耗,并对抗肥胖.

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