除了体温每天的节律性变化外，哺乳动物还能防止它们的核心体温因天气寒冷而降低。

    这项研究发现，核受体Rev-erbR（一个转录抑制因子）通过对棕色脂肪组织功能的调控，充当节律和生热网络与体温节律性之间的一个联系环节。

    暴露于低温的小鼠在上午、当Rev-erbR几乎没有表达时要比在下午几点钟、当Rev-erbR很丰富时状况好得多，而且Rev-erbR基因的删除能提高小鼠对寒冷的耐受力。

    Rev-erbR被发现在棕色脂肪组织中起“去耦合蛋白在在”(Ucp1)的一个生理抑制因子的作用，以此来根据环境情况维持体温节律。

附英文阅读：

The nuclear receptor Rev-erbα controls circadian thermogenic plasticity

Zachary Gerhart-Hines，Dan Feng，Matthew J. Emmett，Logan J. Everett，Emanuele Loro，Erika R. Briggs，Anne Bugge，Catherine Hou，Christine Ferrara，Patrick Seale，Daniel A. Pryma，Tejvir S. Khurana& Mitchell A. Lazar

Circadian oscillation of body temperature is a basic， evolutionarily conserved feature of mammalian biology1. In addition， homeostatic pathways allow organisms to protect their core temperatures in response to cold exposure2. However， the mechanism responsible for coordinating daily body temperature rhythm and adaptability to environmental challenges is unknown. Here we show that the nuclear receptor Rev-erbα (also known as Nr1d1)， a powerful transcriptional repressor， links circadian and thermogenic networks through the regulation of brown adipose tissue (BAT) function. Mice exposed to cold fare considerably better at 05：00 (Zeitgeber time？22) when Rev-erbα is barely expressed than at 17：00 (Zeitgeber time？10) when Rev-erbα is abundant. Deletion of Rev-erbα markedly improves cold tolerance at 17：00， indicating that overcoming Rev-erbα-dependent repression is a fundamental feature of the thermogenic response to cold. Physiological induction of uncoupling protein 1 (Ucp1) by cold temperatures is preceded by rapid downregulation of Rev-erbα in BAT. Rev-erbα represses Ucp1 in a brown-adipose-cell-autonomous manner and BAT Ucp1 levels are high in Rev-erbα-null mice， even at thermoneutrality. Genetic loss of Rev-erbα also abolishes normal rhythms of body temperature and BAT activity. Thus， Rev-erbα acts as a thermogenic focal point required for establishing and maintaining body temperature rhythm in a manner that is adaptable to environmental demands.