RNA-seq of cold-induced transcriptome changes in subcutaneous adipose tissue of beta-adrenergic receptor knockout mice
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Classic brown fat and inducible beige fat both dissipate chemical energy in the form of heat through the actions of mitochondrial uncoupling protein 1. This nonshivering thermogenesis is crucial for mammals as a defense against cold and obesity/diabetes. Cold is known to act indirectly through the sympathetic nervous systems and beta-adrenergic signaling, but here we report that cold temperature can directly activate a thermogenic gene program in adipocytes independent of beta-adrenergic signaling.
经典棕色脂肪与可诱导米色脂肪均通过线粒体解偶联蛋白1(mitochondrial uncoupling protein 1)的介导作用,以热量形式耗散化学能。此类非战栗产热对于哺乳动物抵御寒冷、肥胖及糖尿病而言至关重要。既往研究表明,寒冷可通过交感神经系统(sympathetic nervous systems)与β-肾上腺素能信号通路(beta-adrenergic signaling)间接发挥调控作用,但本研究证实,寒冷温度能够不依赖β-肾上腺素能信号通路,直接激活脂肪细胞(adipocytes)内的产热基因程序。



