一个PPARγ/长非编码RNA轴在小鼠中调节脂肪热中性重塑
Zhengyi Zhang1,2,3, Ya Cui4, Vivien Su1,2,3
1Division of Cardiology, Department of Medicine.
The Journal of clinical investigation
|November 1, 2023
概括
一种新发现的长非编码RNA,Lexis,抑制了白色脂肪组织的散热. 抑制Lexis可以增强发热,抵消肥胖,改善胰岛素敏感性,从而揭示出一种新的PPARγ/WNT通路.
科学领域:
- 脂肪组织生物学 脂肪组织生物学
- 代谢调节 代谢调节 代谢调节
- 分子内分泌学分子内分泌学
背景情况:
- 白色脂肪组织 (WAT) 和色脂肪细胞在肥胖和胰岛素抵抗中相互作用.
- 核受体PPARγ对于脂肪细胞的功能至关重要.
- 将PPARγ与发热与白色脂肪命运联系在一起的机制尚不清楚.
研究的目的:
- 阐明PPARγ在调节WAT命运中的分子机制.
- 研究PPARγ/长非编码RNA (lncRNA) 轴在热生成中的作用.
- 为了确定白色脂肪组织可塑性的新型调节剂.
主要方法:
- 对 lncRNA Lexis 的药理抑制和遗传删除.
- 评估脱蛋白1依赖 (UCP1依赖) 和独立的热生成.
- 单核转录组学和图案分析.
- 在饮食诱导的肥胖模型中的体内研究.
主要成果:
- 雷克西斯删除增强了UCP1依赖和UCP1独立的热生成.
- 特定于脂肪的Lexis删除改善了饮食引起的肥胖,改善了胰岛素敏感性和增加了能量消耗.
- 莱克西斯通过TCF7L2,一种代谢GWAS基因和WNT调节器来调节一个独特的热原性脂肪细胞群.
结论:
- 一个新的PPARγ/lncRNA (Lexis) 轴在热中性和肥胖期间抑制WAT热生成.
- 莱克西斯抑制促进了热生成的表型,提供了潜在的治疗策略.
- 这项研究揭示了PPARγ和WNT信号之间在保持WAT可塑性方面的一种新的交叉声.
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