...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Current Biology: CB >Feeding-State-Dependent Modulation of Temperature Preference Requires Insulin Signaling in Drosophila Warm-Sensing Neurons
【24h】

Feeding-State-Dependent Modulation of Temperature Preference Requires Insulin Signaling in Drosophila Warm-Sensing Neurons

机译：喂养状态依赖性的温度偏好调节需要在果蝇温暖的神经元中的胰岛素信号传导

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Starvation is life-threatening and therefore strongly modulates many aspects of animal behavior and physiology [1]. In mammals, hunger causes a reduction in body temperature and metabolism [2], resulting in conservation of energy for survival. However, the molecular basis of the modulation of thermoregulation by starvation remains largely unclear. Whereas mammals control their body temperature internally, small ectotherms, such as Drosophila, set their body temperature by selecting an ideal environmental temperature through temperature preference behaviors [3, 4]. Here, we demonstrate in Drosophila that starvation results in a lower preferred temperature, which parallels the reduction in body temperature in mammals. The insulin/insulin-like growth factor (IGF) signaling (IIS) pathway is involved in starvation-induced behaviors and physiology and is well conserved in vertebrates and invertebrates [5-7]. We show that insulin-like peptide 6 (Ilp6) in the fat body (fly liver and adipose tissues) is responsible for the starvation-induced reduction in preferred temperature (T-p). Temperature preference behavior is controlled by the anterior cells (ACs), which respond to warm temperatures via transient receptor potential A1 (TrpA1) [4]. We demonstrate that starvation decreases the responding temperature of ACs via insulin signaling, resulting in a lower T-p than in nutrient-rich conditions. Thus, we show that hunger information is conveyed from fat tissues via Ilp6 and influences the sensitivity of warm-sensing neurons in the brain, resulting in a lower temperature set point. Because starvation commonly results in a lower body temperature in both flies and mammals, we propose that insulin signaling is an ancient mediator of starvation-induced thermoregulation.
机译：饥饿是危及生命的，因此强烈调节动物行为和生理学的许多方面[1]。在哺乳动物中，饥饿导致体温和新陈代谢的降低[2]，导致保存能量的生存。然而，通过饥饿调节热调节的分子基础仍然很大程度上不清楚。虽然哺乳动物在内部控制其体温，但通过温度偏好行为选择理想的环境温度，诸如果蝇的小卵巢，例如果蝇[3,4]。在这里，我们在果蝇中证明饥饿导致较低的优选温度，这使得哺乳动物中的体温降低。胰岛素/胰岛素样生长因子（IGF）信号传导（IIS）途径参与饥饿诱导的行为和生理学，并在脊椎动物和无脊椎动物中保存良好[5-7]。我们展示脂肪体（飞肝和脂肪组织中的胰岛素样肽6（ILP6）负责饥饿诱导的优选温度（T-P）。温度偏好行为由前细胞（ACS）控制，前细胞（ACS）通过瞬态受体电位A1（TRPA1）响应温度温度[4]。我们证明饥饿通过胰岛素信号传导降低ACS的响应温度，从而导致富含营养的条件下降。因此，我们表明饥饿信息通过ILP6从脂肪组织传送，并影响大脑中温热感测神经元的敏感性，导致较低的温度设定点。因为饥饿通常导致苍蝇和哺乳动物的较低的体温，我们提出胰岛素信号传导是饥饿诱导的热调节的古老介体。

著录项

  • 来源
    《Current Biology: CB》 |2018年第5期|共12页
  • 作者

    Umezaki Yujiro; Hayley Sean E.; Chu Michelle L.; Seo Hanna W.; Shah Prasun; Hamada Fumika N.;

  • 作者单位

    Cincinnati Childrens Hosp Med Ctr Div Pediat Ophthalmol Abrahamson Pediat Eye Inst Visual Syst Grp 3333 Burnet Ave Cincinnati OH 45229 USA;

    Cincinnati Childrens Hosp Med Ctr Div Pediat Ophthalmol Abrahamson Pediat Eye Inst Visual Syst Grp 3333 Burnet Ave Cincinnati OH 45229 USA;

    Cincinnati Childrens Hosp Med Ctr Div Pediat Ophthalmol Abrahamson Pediat Eye Inst Visual Syst Grp 3333 Burnet Ave Cincinnati OH 45229 USA;

    Cincinnati Childrens Hosp Med Ctr Div Pediat Ophthalmol Abrahamson Pediat Eye Inst Visual Syst Grp 3333 Burnet Ave Cincinnati OH 45229 USA;

    Cincinnati Childrens Hosp Med Ctr Div Pediat Ophthalmol Abrahamson Pediat Eye Inst Visual Syst Grp 3333 Burnet Ave Cincinnati OH 45229 USA;

    Cincinnati Childrens Hosp Med Ctr Div Pediat Ophthalmol Abrahamson Pediat Eye Inst Visual Syst Grp 3333 Burnet Ave Cincinnati OH 45229 USA;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物科学;
  • 关键词

相似文献

  • 外文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号