卡切西亚对瘤携带小鼠骨肌肉蛋白质合成养调节的影响
Brittany R Counts1,2, Quan Zhang1,3, Jessica L Halle1,4
1Integrative Muscle Biology Laboratory, Division of Rehabilitation Sciences, College of Health Professions, University of Tennessee Health Science Center, Memphis, Tennessee, USA.
Journal of cachexia, sarcopenia and muscle
|September 11, 2025
概括
癌症缓冲症加剧了禁食诱导的肌肉消耗反应,而食反应保持完整. 肌肉特异性糖蛋白130 (gp130) 损失会影响禁食时的AMPK激活,但在癌症缓解症期间不会影响蛋白质合成.
科学领域:
- 肌肉生理学和新陈代谢
- 癌症生物学 癌症生物学
- 分子信号通道的分子信号通道.
背景情况:
- 癌症缓解症涉及失调的肌肉蛋白质合成和降解.
- 像mTORC1和AMPK这样的信号通路调节肌肉蛋白平衡.
- 癌症对肌肉蛋白质合成中的食/禁食反应的影响尚不清楚.
研究的目的:
- 研究癌症环境如何通过食和禁食改变骨肌肉蛋白质合成调节.
- 确定通过肌肉糖蛋白130 (gp130) 的IL-6家族细胞因子信号传递是否影响这些反应.
主要方法:
- 在C57BL/6J小鼠中注射了LLC瘤细胞或PBS.
- 小鼠接受了禁食和再食的协议.
- 用AMPK和gp130的肌肉特异性淘汰模型来分析蛋白质表达和合成.
主要成果:
- 在对照和瘤携带的小鼠中,食增加了蛋白质合成,但癌症抑制了整体合成.
- 癌症在养期间加剧了抑制的合成信号传递 (p-AKT).
- 肌肉gp130损失影响了禁食AMPK激活,但并没有抑制癌症小鼠的蛋白质合成.
结论:
- 骨肌中的急性食反应在癌症缓解症期间保持不变,但禁食的代谢反应恶化.
- 肌肉gp130信号传递在禁食期间调节禁食诱导的AMPK激活中发挥作用.
- 需要进一步的研究来了解肌肉AMPK在与癌症相关的蛋白质循环中断中的上游和下游调节.
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