Turyk Mary, Fantuzzi Giamila, Persky Victoria, Freels Sally, Lambertino Anissa, Pini Maria, Rhodes Davina H, Anderson Henry A
University of Illinois at Chicago, Division of Epidemiology and Biostatistics, School of Public Health, 1603 W. Taylor Street, Chicago, IL 60612, United States.
University of Illinois at Chicago, Department of Kinesiology and Nutrition, College of Applied Health Sciences, 1919 W. Taylor Street, Chicago, IL 60612, United States.
Environ Res. 2015 Jul;140:335-44. doi: 10.1016/j.envres.2015.03.037. Epub 2015 Apr 22.
Exposure to persistent organic pollutants (POPs) is associated with increased diabetes risk, although the mechanism of action is not well delineated.
We investigated established diabetes biomarkers that could implicate potential mechanistic pathways, including C-reactive protein (CRP), a marker of systemic inflammation; gamma glutamyl transferase (GGT), a liver enzyme associated with oxidative stress; and adiponectin, an adipokine modulating glucose regulation and fatty acid oxidation. These biomarkers as well as hemoglobin A1c (HA1c), and POPs [polychlorinated biphenyls (PCBs), p,p-dichlorodiphenyldichloroethylene (DDE) and polybrominated diphenyl ethers (PBDEs)] were measured in a cohort of Great Lakes sport caught fish (GLSCF) consumers. We examined associations of POPs and fish consumption with HA1c and incident diabetes, and evaluated mediation and moderation by the diabetes biomarkers.
Odds of incident diabetes were elevated with exposure to DDE and PCBs. DDE and PCB 118 were positively, and fish meals were inversely, associated with HA1c. CRP was inversely associated with saltwater and total fish meals, particularly in persons with higher adiposity, but did not mediate the associations of fish meals with HA1c. There were few associations of POPs with adiponectin, CRP and GGT, with the exception of positive associations of PCB 118 with GGT, PBDEs with GGT in older persons, and PBDEs with adiponectin. Adiponectin, CRP and GGT did not mediate associations of DDE and PCBs with HA1c or incident diabetes. However, the association of DDE with HA1c was stronger in persons with higher CRP, GGT and BMI, and lower adiponectin, while the association of PCB 118 with HA1c was stronger in persons with higher GGT.
These findings suggest that adiponectin, CRP and GGT did not mediate effects of POPs on diabetes or HA1c. However, POPs may have stronger effects on blood glucose in persons at higher risk for diabetes.
接触持久性有机污染物（POPs）与糖尿病风险增加有关，尽管其作用机制尚未完全阐明。
我们研究了一些已确定的糖尿病生物标志物，这些标志物可能涉及潜在的作用机制途径，包括C反应蛋白（CRP），一种全身炎症的标志物；γ-谷氨酰转移酶（GGT），一种与氧化应激相关的肝脏酶；以及脂联素，一种调节葡萄糖代谢和脂肪酸氧化的脂肪因子。在一组食用五大湖捕捞鱼类（GLSCF）的人群中测量了这些生物标志物以及糖化血红蛋白（HA1c）和POPs[多氯联苯（PCBs）、对，对-二氯二苯二氯乙烯（DDE）和多溴二苯醚（PBDEs）]。我们研究了POPs和鱼类消费与HA1c及新发糖尿病之间的关联，并评估了糖尿病生物标志物的中介作用和调节作用。
接触DDE和PCBs会增加新发糖尿病的几率。DDE和多氯联苯118与HA1c呈正相关，而鱼餐与HA1c呈负相关。CRP与海水鱼餐和总鱼餐呈负相关，尤其是在肥胖程度较高的人群中，但CRP并未介导鱼餐与HA1c之间的关联。除了多氯联苯118与GGT呈正相关、老年人中多溴二苯醚与GGT呈正相关以及多溴二苯醚与脂联素呈正相关外，POPs与脂联素、CRP和GGT之间的关联较少。脂联素、CRP和GGT并未介导DDE和PCBs与HA1c或新发糖尿病之间的关联。然而，在CRP、GGT和BMI较高且脂联素较低的人群中，DDE与HA1c的关联更强，而在GGT较高的人群中，多氯联苯118与HA1c的关联更强。
这些发现表明，脂联素、CRP和GGT并未介导POPs对糖尿病或HA1c的影响。然而，POPs可能对糖尿病风险较高的人群的血糖有更强的影响。
