Liu Hong, Wang Jun, Mou Daolin, Che Lianqiang, Fang Zhengfeng, Feng Bin, Lin Yan, Xu Shengyu, Li Jian, Wu De
Institute of Animal Nutrition, Sichuan Agricultural University, No. 211, Huimin Road, Wenjiang District, Chengdu 611130, China.
Nutrients. 2017 Apr 26;9(5):423. doi: 10.3390/nu9050423.
This study was conducted to explore whether exposure to bisphenol A (BPA) during pregnancy could change intestinal digestion and absorption function in offspring using pigs as a model, and whether methyl donor (MET) could counteract the BPA-induced impacts. Fifty Landrace × Yorkshire sows were divided into four dietary groups throughout gestation: control diet (CON); control diet supplemented with BPA (50 mg/kg); control diet supplemented with MET (3 g/kg betaine, 400 mg/kg choline, 150 μg/kg vitamin B12, and 15 mg/kg folic acid); and control diet with BPA and MET supplementation (BPA + MET). Intestine samples were collected from pigs' offspring at birth and weaning. Maternal BPA exposure during pregnancy significantly reduced the ratio of jejunum villus height to crypt depth, decreased the jejunum sucrase activity, down-regulated the mRNA expression of jejunum peptide transporter 1 () and DNA methyl transferase 3a (), and decreased the DNA methylation level of jejunum in offspring ( < 0.05). Maternal MET supplementation significantly raised the ratio of villus height to crypt depth in jejunum and ileum, improved the jejunum lactase activity, up-regulated the mRNA expression of jejunum , lactase (), , , and methylenetetrahydrofolate reductase (), and increased the DNA methylation level of jejunum in offspring ( < 0.05). However, the ratio of jejunum villus height to crypt depth was higher in BPA + MET treatment compared with CON and BPA treatment ( < 0.05). Meanwhile, there was no difference in the jejunum sucrase activity, the mRNA expression of jejunum and , and the DNA methylation level of jejunum between CON and BPA + MET treatment. These results indicated that maternal exposure to BPA during gestation might suppress offspring's intestinal digestion and absorption function, whereas supplementation of MET could counteract these damages, which might be associated with DNA methylation.
本研究旨在以猪为模型，探讨孕期暴露于双酚A（BPA）是否会改变后代的肠道消化吸收功能，以及甲基供体（MET）是否能抵消BPA诱导的影响。50头长白×约克夏母猪在整个妊娠期被分为四个日粮组：对照日粮（CON）；添加BPA（50 mg/kg）的对照日粮；添加MET（3 g/kg甜菜碱、400 mg/kg胆碱、150 μg/kg维生素B12和15 mg/kg叶酸）的对照日粮；以及添加BPA和MET的对照日粮（BPA + MET）。在出生和断奶时从猪的后代收集肠道样本。孕期母体暴露于BPA显著降低了空肠绒毛高度与隐窝深度的比值，降低了空肠蔗糖酶活性，下调了空肠肽转运体1（）和DNA甲基转移酶3a（）的mRNA表达，并降低了后代空肠的DNA甲基化水平（<0.05）。母体补充MET显著提高了空肠和回肠绒毛高度与隐窝深度的比值，改善了空肠乳糖酶活性，上调了空肠、乳糖酶（）、、和亚甲基四氢叶酸还原酶（）的mRNA表达，并提高了后代空肠的DNA甲基化水平（<0.05）。然而，与CON和BPA处理相比，BPA + MET处理的空肠绒毛高度与隐窝深度的比值更高（<0.05）。同时，CON和BPA + MET处理之间的空肠蔗糖酶活性、空肠和的mRNA表达以及空肠的DNA甲基化水平没有差异。这些结果表明，孕期母体暴露于BPA可能会抑制后代的肠道消化吸收功能，而补充MET可以抵消这些损害，这可能与DNA甲基化有关。
