CPEB2-激活Prdm16的翻译促进棕色脂肪细胞的功能,并预防肥胖
Wen-Hsin Lu1, Hui-Feng Chen1, Pei-Chih King1
1Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
Molecular metabolism
|September 21, 2024
概括
细胞质多基化元素结合蛋白2 (CPEB2) 通过控制UCP1和PRDM16的翻译来调节棕色脂肪组织 (BAT) 热生成和体重. 在CPEB2缺乏的小鼠中恢复PRDM16水平可以减轻体重增加.
科学领域:
- 代谢研究的研究.
- 分子生物学分子生物学
- 肥胖研究的研究.
背景情况:
- 棕色脂肪组织 (BAT) 通过解蛋白1 (UCP1) 对热生成至关重要.
- 细胞质多基化元素结合蛋白2 (CPEB2) 之前被确定为UCP1翻译的调节者.
- 缺少CPEB2会导致发热功能受损和肥胖的表型.
研究的目的:
- 为了研究CPEB2控制的翻译对体重调节的影响.
- 阐明CPEB2影响棕色脂肪细胞功能和新陈代谢的机制.
主要方法:
- 全球和条件CPEB2淘汰赛小鼠的体重测量.
- 对缺乏CPEB2的BAT进行RNA测序和生物信息学分析.
- 通过RT-qPCR,Western blotting,多体形分析和光酶测试,证实了CPEB2在PRDM16调节中的作用.
- 在体内通过腺相关病毒 (AAV) 介导的CPEB2或PRDM16的输送.
主要成果:
- 在CPEB2-Knockout (KO) 小鼠中存在BAT功能缺陷,导致体重增加.
- 转录组分析显示,CPEB2-KO的肌肉发育基因受到上调调.
- 通过CPEB2.2,PRDM16的表达被翻译上调调节.
- 在CPEB2-KO BAT中产卵外PRDM16表达恢复了基因表达和减轻体重增加.
结论:
- 通过CPEB2介导的PRDM16的翻译对于维持棕色脂肪细胞功能至关重要.
- CPEB2对棕色脂肪细胞中的热生和代谢活动进行后转录调节.
- 通过对BAT的调节,CPEB2在控制体重方面发挥着至关重要的作用.
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