葡萄糖的新陈代谢与脂肪细胞的热生成有关
Omer Keinan1, Joseph M Valentine1, Haopeng Xiao2,3
1Department of Medicine, University of California San Diego, San Diego, CA, USA.
Nature
|October 28, 2021
概括
脂肪细胞中的糖原代谢对热生成至关重要. 甲基胺调节糖原循环,产生激活p38 MAPK的活性氧物种,驱动解蛋白1 (UCP1) 的表达,从而增加能量消耗.
科学领域:
- 代谢调节
- 蜂能源支出
- 脂肪细胞的功能
背景情况:
- 通过脱蛋白1 (UCP1) 在脂肪细胞中的表达,长时间的交感激活会增加能量消耗.
- 与持续的UCP1表达联系的精确机制尚不完全理解.
研究的目的:
- 研究葡萄糖代谢在调节UCP1表达和脂肪细胞热生成中的作用.
- 阐明连接甲醇胺,糖原和UCP1诱导的信号通路.
主要方法:
- 使用了缺乏蛋白向糖原 (PTG) 的脂肪细胞特异性淘汰小鼠模型.
- 评估糖原水平,UCP1表达,以及对寒冷和β-上腺刺激的热生成反应.
- 分析了反应性氧物种的产生和p38 MAPK的激活.
主要成果:
- 慢性β上腺激活增加了UCP1表达脂肪细胞中的糖原积累.
- 脂肪细胞特异性的PTG删除减少了色脂肪细胞糖原,减弱了UCP1表达,并且导致了寒冷诱导的热生成.
- 催化剂刺激增加了糖原的合成和降解,而糖原的循环需要用于反应性氧物种的产生和p38 MAPK的激活,这驱动了UCP1的表达.
结论:
- 葡萄糖代谢在脂肪细胞热生成中起着关键的调节作用.
- 通过活性氧物种和p38 MAPK信号,糖代谢与UCP1介导的能量消耗相联系.
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