禁食增加了循环中的血管素水平和大脑Agtr1a表达在雄性大鼠
Bruno Paes-Leme1, Lívia da Rocha Natalino Monteiro1, Khadijeh Gholami2
1Department of Physiological Sciences, Institute of Biological and Health Sciences, Federal Rural University of Rio de Janeiro, Seropédica, Rio de Janeiro, Brazil.
Journal of neuroendocrinology
|September 5, 2023
概括
禁食会增加氨酸 - 血管酶系统 (RAS) 的活性,影响大脑的信号传递. 在禁食后重新养期间,作用于下器官 (SFO) AT1受体的 ангиотензин II (ANG II) 可能会调节口渴.
科学领域:
- 神经内分泌学神经内分泌学
- 代谢生理学 代谢生理学
- 心血管监管 监管心血管系统
背景情况:
- 氨酸 - ангиотензин 系统 (RAS) 对于心血管和水矿物质平衡至关重要.
- RAS,特别是血管激素II (ANG II) /1型受体 (AT1R) 在下器官 (SFO) 中的信号传递,与能量平衡控制有关.
- SFO集成了自主功能,动机行为和能量代谢.
研究的目的:
- 调查循环中的ANG II是否与SFO AT1R相互作用,以整合代谢和水矿物平衡.
- 评估食物剥夺对系统RAS活动和大脑 ангиотензиноген (Agt) mRNA表达的影响.
- 为了确定 ANG II/AT1R 信号传导如何影响大脑下丘脑神经的表达和大鼠的饮食行为.
主要方法:
- 大鼠接受了24小时和48小时的禁食期.
- 测量了 ANG I 和 ANG II 的血水平.
- 分析了AgtmRNA在SFO和副腹腔核 (PVN) 中的表达.
- 老鼠在饮用水中或通过脑内静脉注射接受了洛萨坦 (AT1R抗剂).
- 评估了食物和水摄入量,血糖和下丘脑神经的mRNA水平.
主要成果:
- 禁食显著提高了血ANG I和ANG II水平.
- 食物剥夺在SFO和PVN中增加了Agt mRNA表达.
- 在禁食大鼠中,洛萨坦治疗减轻了禁食诱导的低血糖症,并在重新养期间减少了口渴.
- 食老鼠在黑暗阶段的食老鼠中,食食老鼠的食物和水摄入量有所降低,但在禁食老鼠中却没有降低.
结论:
- 在SFO AT1R信号上作用的外围ANG II在控制再养引起的口渴方面发挥着作用.
- 中央ANG II/AT1R信号影响饮食和饮酒行为以状态依赖的方式 (食与禁食).
- 该研究强调了RAS在代谢挑战期间整合能量和水矿物平衡方面的复杂作用.
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