在禁食期间,蛋白质体调节人体体重和全身营养代谢
Henning Tim Langer1, Samuel R Taylor1, Mujmmail Ahmed1
1Department of Medicine, Weill Cornell Medicine, New York, New York, United States.
American journal of physiology. Endocrinology and metabolism
|September 6, 2023
概括
用博特佐米布抑制全素-蛋白酶体系统 (UPS) 可以防止在禁食期间身体和组织的体重减轻. 这种蛋白酶抑制也增强了禁食诱导的生成,并促进了肝脏蛋白质的合成.
科学领域:
- 代谢调节 代谢调节 代谢调节
- 细胞降解途径 细胞降解途径
- 生物化学 生物化学
背景情况:
- 无素-蛋白酶体系统 (UPS) 和自-溶酶体通路是哺乳动物的关键降解机制.
- 对于代谢研究来说,了解它们在禁食期间的代谢过程中的不同作用至关重要.
研究的目的:
- 为了确定UPS和自细胞在15小时的夜间禁食期间对组织代谢的个人贡献.
- 研究UPS抑制对全身新陈代谢和组织降解的影响.
主要方法:
- 小鼠接受过夜禁食,有或没有干预:克洛洛昆 (自抑制剂) 或博特佐米布 (UPS抑制剂).
- 评估的体重,组织质量,循环的荷尔蒙/代谢物,细胞内信号和蛋白质合成.
- 评估肝脏UPS抑制和PI3K/AKT/mTOR通路的激活.
主要成果:
- 禁食导致身体和组织的体重减轻,而这种减轻是由博尔特佐米布治疗预防的.
- 博尔特佐米布治疗加剧了禁食诱导的生成,并增加了循环中的β-基酸盐水平.
- 抑制UPS可以提高肝脏PI3K/AKT/mTOR信号的调节,促进蛋白质合成.
结论:
- 通过博尔特佐米布抑制UPS有效地阻断了小鼠在急性禁食期间的体重减轻和组织代谢.
- 这些影响很可能是由于生物分子降解减少和合成增强的结合.
- 禁食期间的博特佐米布治疗增加了肝脏的AMPK和PI3K/AKT信号,促进了蛋白质合成.
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