核心压缩器NRIP1和cAMP信号在脂肪细胞热生成编程上的交叉声
Emmanouela Tsagkaraki1, Adilson Guilherme1, Sarah M Nicoloro1
1Program in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA.
Molecular metabolism
|July 23, 2023
概括
在脂肪细胞中削弱核受体相互作用蛋白1 (NRIP1) 增加了整个身体的新陈代谢和能量消耗,当植入肥胖小鼠时. 这种效应是独立的,但与cAMP途径合作,用于脂肪细胞的化.
科学领域:
- 代谢调节 代谢调节 代谢调节
- 脂肪细胞生物学 脂肪细胞生物学
- 肥胖研究的研究.
背景情况:
- 核受体相互作用蛋白1 (NRIP1) 通过抑制核受体来调节能量消耗.
- NRIP1的枯竭增加了脂肪细胞的脱呼吸,这表明它在热生成中发挥了作用.
研究的目的:
- 为了研究NRIP1缺乏脂肪细胞是否增强肥胖小鼠的全身新陈代谢.
- 为了确定NRIP1淘汰赛 (NRIP1KO) 对脂肪细胞热生成的影响是否取决于cAMP通路.
主要方法:
- NRIP1KO脂肪细胞植入高脂肪饮食 (HFD) 接受者小鼠.
- 使用CRISPR在来自对照和GsαKO小鼠的脂肪细胞中进行了对Nrip1的基因破坏.
- 使用了代谢研究和药理干预 (蛋白激酶A抑制剂,CL 316,243).
主要成果:
- 对NRIP1KO脂肪细胞的植入改善了接受者小鼠的葡萄糖耐受性,减少了脂肪性,并增加了能量消耗.
- NRIP1 枯竭高调解离合蛋白 1 (UCP1) 和脂肪细胞独立于cAMP通路.
- 将NRIP1KO与β-上腺刺激相结合,协同增强了Ucp1的表达和表达.
结论:
- 在脂肪细胞中NRIP1的耗尽促进了转移到肥胖宿主时的全身能量消耗.
- NRIP1KO的热能效应是独立的,但与脂肪细胞中cAMP通路的合作.
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