Environmental Research ( IF 7.7 ) Pub Date : 2023-10-18 , DOI: 10.1016/j.envres.2023.117410 Weiya Li 1 , Zhaoyang Li 1 , Yan Yan 1 , Jiazhen Zhang 1 , Qihang Zhou 1 , Ruixin Wang 1 , Meian He 1
Background
Previous researches have assessed the relationships of urinary arsenic metabolism with type 2 diabetes (T2D) and glucose-insulin homeostasis, but the results were controversial, and potential mechanisms remain largely unclear.
Objectives
This study aimed to investigate the cross-sectional and longitudinal associations of urinary arsenic metabolism with T2D prevalence and glucose changes in relatively higher arsenic exposure, and further to evaluate the underlying roles of oxidative damage in these relationships.
Methods
We included 796 participants at baseline, among them 509 participants were followed up after 2 years. Logistic regression model and leave-one-out approach were applied to evaluate the associations of arsenic metabolism with T2D prevalence. Linear mixed model was conducted to estimate the relationship of arsenic metabolism with glycemic changes over two years. The associations between arsenic metabolism and indicators of oxidative stress were assessed with a linear regression model. We further performed mediation analysis to investigate the role of oxidative stress in the associations of arsenic metabolism with 2-year change of glucose levels.
Results
Higher urinary MMA% increased T2D prevalence and baseline glucose levels. MMA% was positively associated with 2-year change of glucose levels. Moreover, we observed significant dose-response relationship between MMA% and 8-hydroxy-2-deoxyguanosine (8-OHdG). However, the mediating role of 8-OHdG in the association of MMA% and 2-year change of glucose levels was not observed in this population.
Conclusions
In this population exposure to relatively higher arsenic levels, higher MMA% contributed to increased T2D prevalence and glucose homeostasis disorder. Arsenic metabolism also affected oxidative stress levels, especially 8-OHdG. Further studies are required to investigate the potential mechanisms.
中文翻译:
尿砷代谢与 2 型糖尿病和葡萄糖稳态的关联:横断面和纵向关联。
背景
以前的研究评估了尿砷代谢与 2 型糖尿病 (T2D) 和葡萄糖-胰岛素稳态的关系,但结果存在争议,潜在机制在很大程度上仍不清楚。
目标
本研究旨在调查尿砷代谢与 T2D 患病率和相对较高的砷暴露量下的葡萄糖变化的横断面和纵向关联,并进一步评估氧化损伤在这些关系中的潜在作用。
方法
我们纳入了 796 名基线参与者,其中 509 名参与者在 2 年后进行了随访。应用 Logistic 回归模型和留一法评估砷代谢与 T2D 患病率的相关性。采用线性混合模型估计两年内砷代谢与血糖变化的关系。用线性回归模型评估砷代谢与氧化应激指标之间的关联。我们进一步进行了中介分析,以研究氧化应激在砷代谢与 2 年葡萄糖水平变化的关系中的作用。
结果
较高的尿 MMA% 增加了 T2D 患病率和基线血糖水平。MMA% 与血糖水平 2 年变化呈正相关。此外,我们观察到 MMA% 和 8-羟基-2-脱氧鸟苷 (8-OHdG) 之间存在显着的剂量反应关系。然而,在该人群中未观察到 8-OHdG 在 MMA% 和 2 年葡萄糖水平变化相关性中的中介作用。
结论
在这个暴露于相对较高的砷水平的人群中,较高的 MMA% 导致 T2D 患病率和葡萄糖稳态障碍增加。砷代谢也影响氧化应激水平,尤其是 8-OHdG。需要进一步的研究来调查潜在的机制。