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The nuclear receptor Rev-erbα controls circadian thermogenic plasticity

机译：核受体Rev-erbα控制昼夜节律的可塑性

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摘要

Circadian oscillation of body temperature is a basic, evolutionarily conserved feature of mammalian biology. In addition, homeo-static pathways allow organisms to protect their core temperatures in response to cold exposure. 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-erba (also known as Nrldl), 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-erba is barely expressed than at 17:00 (Zeitgeber time 10) when Rev-erba is abundant. Deletion of Rev-erba markedly improves cold tolerance at 17:00, indicating that overcoming Rev-erba-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-erba in BAT. Rev-erba 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-erba also abolishes normal rhythms of body temperature and BAT activity. Thus, Rev-erba acts as a thermogenic focal point required for establishing and maintaining body temperature rhythm in a manner that is adaptable to environmental demands.%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-erbα (—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-erba几乎没有表达时要比在下午5点钟、当Rev-erbα很丰富时状况好得多，而且Rev-erbα基因 的删除能提高小鼠对寒冷的耐受力。Rev-erbα被发现在棕色脂肪组织中起"去耦合蛋白-1"(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。
机译：体温的昼夜节律振荡是哺乳动物生物学的一个基本的，进化上保守的特征。此外，稳态途径可以使生物保护自身的核心温度以应对冷暴露。然而，负责协调日常体温节律和适应环境挑战的机制尚不清楚。在这里，我们显示核受体Rev-erba（也称为Nrldl），一种功能强大的转录阻遏物，通过调节棕色脂肪组织（BAT）的功能来连接昼夜节律和产热网络。当Rev-erba很少表达时，小鼠在05:00（Zeitgeber时间22）暴露于冷票价要好于Rev-erba丰富的17:00（Zeitgeber时间10）。 Rev-erba的删除显着提高了17:00时的耐寒性，这表明克服Rev-erba依赖性抑制是热源对寒冷的反应的基本特征。在低温下，生理上诱导解偶联蛋白1（Ucp1）的过程是BAT中Rev-erba迅速下调。 Rev-erba以棕色脂肪细胞自主方式抑制Ucp1，即使在热中性下，Rev-erbα-null小鼠的BAT Ucp1水平也很高。 Rev-erba的遗传丧失也消除了体温和BAT活性的正常节律。因此，Rev-erba成为建立和维持体温节律所需的产热焦点，且适应环境需求。％除了体温每天的节律性变化外，其他避免其自身的核心体温因天气研究发现，核受体Rev-erbα（—一个转录抑制因子）通过对棕色姨妈组织功能的转变，替代节律和生热网络与体温节律性之间的一个联系中断。暴露于。低温的小鼠在上午，当Rev-erba几乎没有表达时要比在下午5点钟，当Rev-erbα很丰富时状况好解决，而且Rev-erbα基因的删除能提高小鼠对寒冷的耐受力。Rev-erbα被发现在棕色成年人组织中起“去重组蛋白-1”（Ucp1）的一个生理抑制因子的作用，从而根据环境情况维持体温节律。

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  • 来源
    《Nature》 |2013年第7476期|410-413a5|共5页
  • 作者

    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;

  • 作者单位

    Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA,The Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;

    Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA,The Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;

    Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA,The Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;

    Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA,The Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;

    Department of Physiology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA,Pennsylvania Muscle Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;

    Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA,The Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;

    Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA,The Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;

    Department of Radiology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;

    Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA;

    The Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA,Department of Cell and Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;

    Department of Radiology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;

    Department of Physiology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA,Pennsylvania Muscle Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;

    Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA,The Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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