与2型糖尿病有关的多基因风险和空气污染趋势:来自台湾生物银行的证据
Osama Aziz1, Bing-Fang Hwang2, Ai-Ru Hsieh3
1Department of Public Health, College of Public Health, China Medical University, No. 100, Sec. 1, Jingmao Rd. Beitun Dist., Taichung, 406040, Taiwan.
Diabetology & metabolic syndrome
|January 20, 2026
概括
空气污染,特别是细颗粒物 (PM2.5) 和高遗传风险得分与2型糖尿病 (T2D) 有关. 虽然PM2.5暴露与T2D遗传风险的相互作用很弱,但这两种因素独立地增加了疾病风险.
科学领域:
- 环境健康 环境健康
- 遗传学 遗传学 是一个
- 流行病学 流行病学
背景情况:
- 遗传倾向和空气污染是已知的2型糖尿病 (T2D) 的风险因素.
- 亚洲人群中空气污染暴露和对T2D的遗传易感性之间的相互作用尚未得到充分理解.
- 本研究研究了特定空气污染物 (PM2.5,NO2,SO2,O3) 和T2D风险之间的关联,并纳入多基因风险评分 (PRS).
研究的目的:
- 评估暴露于常见空气污染物和T2D风险之间的关联.
- 评估多基因风险评分 (PRS) 在T2D易感性中的作用.
- 在亚洲队列中检查空气污染和T2D遗传风险之间的潜在基因环境相互作用.
主要方法:
- 利用了台湾生物库的104,554名参与者的数据.
- 使用卫星模型估计空气污染物度,并分析长期趋势.
- 从东亚GWAS数据构建了T2D特定的多基因风险评分 (PRS),并使用后勤回归来分析关联和相互作用.
主要成果:
- 增加PM2.5度 (每年1μg/m3) 与增加T2D风险 (OR:1.036) 有显著关联.
- 较高的PRS四分位数显示出与T2D风险的阳性暴露-反应关系,最高四分位数显示显著增加风险 (OR: 1.385).
- 在PM2.5暴露趋势和T2D高遗传风险之间观察到一个微弱的,边界显著的添加物相互作用.
结论:
- 增加的PM2.5暴露和升高的PRS都与T2D独立相关.
- 关于T2D风险的PM2.5和PRS之间的相互作用很弱,需要谨慎解释.
- 调查结果强调了改善空气质量和个性化预防对于具有高遗传易感性T2D的个体的重要性.
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