在脂肪细胞中PPARγ乙化 加剧BAT白化并恶化与年龄相关的代谢功能障碍
Ying He1,2, Ruotong Zhang1,2, Lexiang Yu1,2
1Naomi Berrie Diabetes Center, Columbia University, New York, NY 10032, USA.
Cells
|July 6, 2023
概括
衰老和肥胖会使代谢功能障碍恶化,这是由于PPARγ过乙化. 一种新的小鼠模型表明,这种乙化会损害棕色脂肪的功能,并加剧代谢问题,突出显示PPARγ是治疗点.
科学领域:
- 代谢性疾病是一种代谢性疾病.
- 分子生物学分子生物学
- 衰老的研究研究.
背景情况:
- 衰老和肥胖是代谢功能障碍的关键驱动因素,不清楚的共享机制.
- 过氧体增殖器激活受体玛 (PPARγ),一个代谢调节器和胰岛素耐药性标,在衰老和肥胖中被过度乙化.
研究的目的:
- 调查脂肪细胞PPARγ乙化在衰老期间代谢功能障碍中的作用.
- 探索PPARγ乙化对棕色脂肪组织 (BAT) 功能和治疗干预措施的影响.
主要方法:
- 使用了一种新的脂肪细胞特异PPARγ乙化模仿突变突击鼠标模型 (aKQ).
- 评估代谢参数 (肥胖,胰岛素耐药性,脂质不良,葡萄糖不耐受) 与衰老和干预措施 (间歇性禁食,TZD,白醇).
- 分析了棕色脂肪组织 (BAT) 现型和标记物,以及骨损失的影响.
主要成果:
- aKQ小鼠表现出加速肥胖,胰岛素耐药性,脂质障碍症和葡萄糖不耐受,随着年龄的增长,对间歇性禁食没有反应.
- 在aKQ小鼠中观察到BAT (脂质积累,抑制标记物) 中的"白化"表型,尽管激活了SirT1,但仍然存在.
- 对于饮食诱导的肥胖症,TZD治疗的疗效保持不变,但未能恢复BAT功能;在aKQ小鼠中,骨损失恶化.
结论:
- 脂肪细胞PPARγ乙化对与衰老相关的代谢功能障碍有病原性影响.
- PPARγ乙化损害了BAT功能,并加剧了代谢和骨质损失问题.
- 向脂肪细胞PPARγ乙化是一种潜在的代谢障碍治疗策略.
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