通过calsyntenin 3β-S100b轴激活发热脂肪组织
Xing Zeng1,2, Mengchen Ye3, Jon M Resch4
1Department of Cancer Biology, Dana Farber Cancer Institute, Boston, MA, USA.
Nature
|May 3, 2019
概括
热性脂肪细胞通过一种新型蛋白质calsyntenin 3β与交感神经元进行通信. 这种相互作用调节脂肪热生成,并保护小鼠免受饮食引起的肥胖.
科学领域:
- 代谢过程
- 神经内分泌学
- 细胞生物学
背景情况:
- 交感神经系统通过上腺素调节棕色和色脂肪细胞的热生成.
- 在热生成脂肪中增加的交感内置背后的分子机制尚不清楚.
研究的目的:
- 调查热生成脂肪细胞增强的交感内置的分子基础.
- 识别脂肪细胞和交感神经元之间的通信中的新因素.
主要方法:
- 在脂肪细胞中利用了calsyntenin 3β的基因操纵 (功能损失和增益).
- 在脂肪组织中评估了同情性内化.
- 在实验室中分析了calsyntenin 3β对S100b分泌的作用及其对交感神经元的影响.
- 研究了素3β缺乏对小鼠饮食引起的肥胖的影响.
主要成果:
- 在热性脂肪细胞中鉴定出素3β,一种哺乳动物特异性的内等质网膜蛋白.
- 在脂肪组织中改变了calsyntenin 3β的遗传调节.
- 素3β促进S100b的分泌,从而刺激交感神经元的生长.
- 在高脂肪饮食的小鼠中,素3β的消去导致肥胖,从而导致S100b缺乏.
结论:
- 发现了一种新型的哺乳动物特异性机制,其中calsyntenin 3β调解热生成脂肪细胞和交感神经元之间的通信.
- 氨酸3β-S100b通路对于调节交感内置和预防肥胖至关重要.
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