健康和肥胖小鼠肝脏中对饥饿反应代谢网络的结构稳定性和时间脆弱性
Keigo Morita1,2, Atsushi Hatano1,3,4, Toshiya Kokaji1,5
1Department of Biological Sciences, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan.
Science signaling
|April 22, 2025
概括
健康的肝脏在饥饿期间通过ATP和AMP等枢纽分子暂时协调新陈代谢. 肥胖会破坏这个时间秩序,尽管有结构强大的代谢网络,但会损害饥饿反应.
科学领域:
- 代谢调节 代谢调节 代谢调节
- 系统生物学 系统生物学
- 肥胖研究的研究.
背景情况:
- 饥饿适应是一个复杂的,时间依赖的过程,涉及多个分子.
- 了解肝脏如何调节对饥饿的代谢反应对于代谢健康至关重要.
- 众所周知,肥胖会破坏正常的生理过程,但其对饥饿适应的具体影响需要进一步阐明.
研究的目的:
- 为了研究肝脏分子在饥饿期间的时间调节,在健康和肥胖状态下.
- 确定饥饿适应中的关键分子参与者和网络动态.
- 了解肥胖症,特别是瘦素缺乏的小鼠,如何破坏这些时间代谢过程.
主要方法:
- 在饥饿期间从野生类型和肥胖 (ob/ob) 小鼠获得的多分子数据 (血和肝脏).
- 建立一个对饥饿反应的代谢网络,包括监管关系.
- 网络结构和时间动态分析,专注于ATP和AMP等枢纽分子.
主要成果:
- 在野生类型的小鼠中,ATP和AMP充当了中央枢纽分子,协调了暂时有序的代谢反应.
- 肥胖 (ob/ob) 的小鼠表现出ATP和AMP对饥饿反应的损失,但网络的结构仍然完好无损.
- 与野生类型相比,肥胖小鼠的时间顺序和代谢分子的协同调节显著受到干扰.
结论:
- 饥饿反应代谢网络在结构上很强大,但暂时容易受到肥胖的影响.
- 肥胖症中枢分子响应能力 (ATP,AMP) 的丧失导致对饥饿的时间适应受损.
- 肥胖会通过破坏时间代谢协调来改变肝脏对间歇性禁食的反应.
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