高脂肪饮食和PM2.5暴露于代谢异常肥胖的分子途径:系统性审查和元分析
Sagrario Lobato1,2,3, Víctor Manuel Salomón-Soto3, Claudia Magaly Espinosa-Méndez4
1Departamento de Investigación en Salud, Servicios de Salud del Estado de Puebla, 603 North 6th Street, Centro Colony, Puebla 72000, Mexico.
Biomolecules
|January 8, 2025
概括
对高脂肪饮食和细颗粒物 (PM2.5) 的联合暴露显著放大了肥胖和代谢功能障碍. 这种协同作用会加剧体重增加和氧化应激,影响整体代谢健康.
科学领域:
- 环境健康 环境健康
- 代谢科学 代谢科学
- 毒理学 毒理学 毒理学
背景情况:
- 肥胖是一种复杂的疾病,受到环境因素的影响,包括污染物.
- 代谢异常的肥胖症可能是由饮食和环境因素的联合暴露引起的.
- 微粒颗粒物 (PM2.5) 是一个重要的环境污染物,与不利的健康结果有关.
研究的目的:
- 系统地审查和分析由高脂肪饮食 (HFD) 和PM2.5暴露引起的代谢异常肥胖的分子机制.
- 进行对HFD和PM2.5对代谢健康的综合影响现有研究的元分析.
- 确定这些联合暴露影响的关键生物途径.
主要方法:
- 在Scopus,科学网络和PubMed (2019-2024) 进行了系统的文献搜索.
- 随机效应的元分析,子组分析,以及按照PRISMA指导方针进行的途径丰富分析.
- 包括33篇文章,主要是病例控制研究和小鼠模型.
主要成果:
- 结合HFD和PM2.5暴露导致最大的体重增加 (82.835g,p=0.048).
- 观察到高密度脂蛋白,胰岛素和超氧化物失调酶的水平增加.
- HFD影响了棕色脂肪组织中的脂肪基因信号传递;PM2.5影响了脂肪形成基因;降低了白色脂肪组织中的蛋白质代谢,并激活了心脏应激反应.
- 肝脏中的丰富途径包括PPAR和AMPK信号传递,影响非酒精性脂肪肝疾病.
结论:
- 结合HFD和PM2.5暴露,协同增强了体重增加和氧化应激.
- 这些暴露会引起显著的代谢功能障碍,包括对脂质代谢和肝脏健康的影响.
- 这些发现强调了在代谢健康干预中考虑环境和饮食暴露的关键性.
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