Debost-Legrand Anne, Warembourg Charline, Massart Catherine, Chevrier Cécile, Bonvallot Nathalie, Monfort Christine, Rouget Florence, Bonnet Fabrice, Cordier Sylvaine
National Institute of Health and Medical Research (Inserm), U1085, Institut de Recherche en Santé, Environnement et Travail (Irset), F-35043 Rennes, France; Centre Hospitalier Universitaire de Clermont-Ferrand, Service de Santé Publique, F-63000 Clermont-Ferrand, France; Centre Hospitalier Universitaire de Clermont-Ferrand, EA 4681, PEPRADE, Université d'Auvergne, F- 63000 Clermont-Ferrand, France.
National Institute of Health and Medical Research (Inserm), U1085, Institut de Recherche en Santé, Environnement et Travail (Irset), F-35043 Rennes, France; Université de Rennes I, F-35043 Rennes, France.
Environ Res. 2016 Apr;146:207-17. doi: 10.1016/j.envres.2016.01.005. Epub 2016 Jan 11.
Experimental evidence suggests that developmental exposure to persistent organic pollutants (POP) and to some non persistent pesticides may disrupt metabolic regulation of glucose metabolism and insulin secretion, and thereby contribute to the current epidemic of obesity and metabolic disorders. Quasi-experimental situations of undernutrition in utero have provided some information. However, the evidence in humans concerning the role of the prenatal environment in these disorders is contradictory, and little is known about long-term outcomes, such as type 2 diabetes, of prenatal exposure.
Our aim was to evaluate the effects of prenatal exposure to POP and organophosphate pesticides on fetal markers of glucose metabolism in a sample of newborns from the Pelagie mother-child cohort in Brittany (France).
Dialkylphosphate (DAP) metabolites of organophosphate pesticides were measured in maternal urine collected at the beginning of pregnancy. Cord blood was assayed for polychlorinated biphenyl congener 153 (PCB153), p,p'-dichlorodiphenyl dichloroethene (DDE) and other POP. Insulin and adiponectin were determined in cord blood serum (n=268).
A decrease in adiponectin and insulin levels was observed with increasing levels of DDE, but only in girls and not boys. Adiponectin levels were not related to the concentrations of other POP or DAP metabolites. Decreasing insulin levels were observed with increasing PCB153 concentrations. Insulin levels increased with DAP urinary levels. Additional adjustment for BMI z-score at birth modified some of these relations.
Our observations bring support for a potential role of organophosphate pesticides and POP in alterations to glucose metabolism observable at birth.
实验证据表明，发育过程中接触持久性有机污染物（POP）和某些非持久性农药可能会扰乱葡萄糖代谢和胰岛素分泌的代谢调节，从而导致当前肥胖和代谢紊乱的流行。子宫内营养不良的准实验情况提供了一些信息。然而，关于产前环境在这些疾病中的作用，人类的证据相互矛盾，而且对于产前接触的长期后果，如2型糖尿病，知之甚少。
我们的目的是评估产前接触POP和有机磷农药对法国布列塔尼佩拉吉母婴队列中新生儿葡萄糖代谢胎儿标志物的影响。
在怀孕初期收集的孕妇尿液中测量有机磷农药的二烷基磷酸酯（DAP）代谢物。检测脐带血中的多氯联苯同系物153（PCB153）、p,p'-二氯二苯二氯乙烯（DDE）和其他POP。测定脐带血血清中的胰岛素和脂联素（n = 268）。
随着DDE水平的升高，脂联素和胰岛素水平降低，但仅在女孩中出现，男孩中未出现。脂联素水平与其他POP或DAP代谢物的浓度无关。随着PCB153浓度的升高，胰岛素水平降低。胰岛素水平随尿液中DAP水平升高而升高。对出生时BMI z评分进行额外调整后，改变了其中一些关系。
我们的观察结果支持有机磷农药和POP在出生时可观察到的葡萄糖代谢改变中可能发挥的作用。
