Persistent organic pollutants and biomarkers of diabetes risk in a cohort of Great Lakes sport caught fish consumers.

Persistent organic pollutants and biomarkers of diabetes risk in a cohort of Great Lakes sport caught fish consumers.
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DOI:
10.1016/j.envres.2015.03.037
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发表时间:
2015-07
影响因子:
8.3
通讯作者:
Anderson, Henry A.
Anderson, Henry A.
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Turyk, Mary;Fantuzzi, Giamila;Persky, Victoria;Freels, Sally;Lambertino, Anissa;Pini, Maria;Rhodes, Davina H.;Anderson, Henry A.

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暴露于持久性有机污染物(POPs)与糖尿病风险增加有关,尽管其作用机制尚未很好地描述。我们研究了已建立的可能涉及潜在机制途径的糖尿病生物标记物,包括全身炎症的标记物C-反应蛋白(CRP);与氧化应激相关的肝酶伽马谷氨酰转移酶(GGT);以及调节葡萄糖调节和脂肪酸氧化的脂肪因子脂联素。这些生物标志物以及血红蛋白A1c(HA1c)和POPs[多氯联苯(PCBS)、对二氯二苯基二氯乙烯(DDE)和多溴联苯醚(PBDEs)]在五大湖捕捞鱼类(GLSCF)消费者的队列中进行了测量。我们研究了持久性有机污染物和鱼类消费与HA1c和糖尿病事件的关系,并评估了糖尿病生物标记物的调节和缓和作用。接触DDE和多氯联苯会增加患糖尿病的几率。DDE和PCB118与HA1c呈正相关,鱼粉与HA1c呈负相关。C反应蛋白与盐水和总鱼粉呈负相关,特别是在肥胖度较高的人中,但不能调节鱼粉与HA1c的关联。除了老年人中GGT与多氯联苯118和多溴联苯醚呈正相关,以及脂联素与多溴二苯醚呈正相关外,脂联素、C反应蛋白和GGT与持久性有机污染物几乎没有关联。脂联素、C反应蛋白和GGT不能调节DDE和多氯联苯与HA1c或糖尿病发病的关系。然而,在CRP、GGT、BMI较高和脂联素较低的人群中,DDE与HA1c的关联较强,而PCB118与HA1c的关联在GGT较高的人群中较强。这些发现表明,脂联素、C反应蛋白和GGT不能介导POPS对糖尿病或糖化血红蛋白的影响。然而,持久性有机污染物可能对糖尿病高危人群的血糖有更强的影响。
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 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 adiponectin, CRP and GGT with POPs, with the exception of positive associations of GGT with PCB 118 and with PBDEs in older persons, and a positive association of adiponectin with PBDEs. 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.
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