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对过度养引起的体重增加的保护在肥胖中保持,但不需要FGF21或MC4RR
Camilla Lund1, Pablo Ranea-Robles1, Sarah Falk1
1Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark.
Nature communications
|February 8, 2024
概括
身体通过减少食物摄入量来防御体重增加,即使在肥胖中也是如此. 这种防御涉及腿骨蛋白 (LGMN) 和下丘脑信号,独立于FGF21和MC4R.
科学领域:
- 代谢和内分泌学
- 肥胖问题研究研究
- 神经科学是一个神经科学.
背景情况:
- 恒温机制抵消了过度养后的体重增加.
- 饮食诱导的肥胖 (DIO) 模型对于研究体重调节至关重要.
- 了解重量恢复所涉及的分子途径至关重要.
研究的目的:
- 调查超量养引起的瘦肉和DIO小鼠体重增加的补偿机制.
- 为了确定参与防御体重增加的新型循环因素.
- 探索下丘脑信号传递和特定受体在体重恢复中的作用.
主要方法:
- 在瘦肉和DIO雄性小鼠中过度养的方案.
- 有针对性的蛋白质组学来识别循环因素.
- 在DIO小鼠中使用复合豆类素 (LGMN).
- 脑下垂体血管化和神经基因表达的分析 (Npy,Agrp).
- 在黑色皮质素4受体 (MC4R) 淘汰小鼠中的过度养研究.
主要成果:
- 瘦肉和DIO小鼠都显示出过度养后对食物摄入的强烈抑制.
- 发现FGF21对于这种防御机制是不可或缺的.
- 标识Legumain (LGMN) 是一种新型循环因子,可以降低DIO小鼠的体重和食物摄入量.
- 观察到下丘脑血管缩小和持续抑制氧化神经 (Npy,Agrp) 的情况.
- MC4R淘汰赛小鼠可以抑制食物摄入,但体重恢复受损.
结论:
- 对过度养引起的体重增加的防御在肥胖中是完整的.
- 这种防御涉及独立于FGF21和MC4R的机制.
- 腿筋蛋白 (LGMN) 和下丘脑信号通路在抵消体重增加方面发挥着重要作用.
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