Effects of Maternal LPS Exposure during Pregnancy on Metabolic Phenotypes in Female Offspring
Effects of Maternal LPS Exposure during Pregnancy on Metabolic Phenotypes in Female Offspring
复制标题
怀孕期间母体 LPS 暴露对女性后代代谢表型的影响
DOI：
10.1371/journal.pone.0114780
复制
发表时间：
2014-12-05
期刊：
影响因子：
3.7
通讯作者：
Xu, De-Xiang
中科院分区：
文献类型：
--
作者：
Liu, Xiao-Jing;Wang, Bi-Wei;Xu, De-Xiang
人们越来越认识到，宫内生长受限（IUGR）与晚年代谢紊乱风险增加有关。以往的研究表明，小鼠在妊娠晚期暴露于LPS可诱发胎儿IUGR。本研究调查了母体妊娠期间暴露于LPS对雌性成年后代代谢表型的影响。妊娠小鼠从妊娠第15天（GD）至GD 17天每天腹腔注射LPS（50 µg/kg）。哺乳后，雌性幼仔饲喂标准饲料（SD）或高脂饲料（HFD）。在饮食干预后8周和12周进行葡萄糖耐量试验（GTT）和胰岛素耐量试验（ITT）。饮食干预12周后检测肝脏甘油三酯含量。正如预期的那样，母体在妊娠期间暴露于LPS导致胎儿IUGR。妊娠期暴露于LPS的母鼠，其雌性子代的脂肪量有增加的趋势，但母鼠妊娠期暴露于LPS并没有使雌性成年子代的空腹血糖、血清胰岛素和肝脏甘油三酯含量升高。此外，母体在怀孕期间暴露于LPS并没有改变雌性成年后代脂肪组织和肝脏中的胰岛素敏感性。进一步的分析表明，母体在怀孕期间暴露于LPS不会加重HFD诱导的雌性成年后代的葡萄糖耐量和胰岛素抵抗。此外，母体LPS暴露在怀孕期间并没有加剧HFD诱导的升高肝脏甘油三酯含量的雌性成年后代。总之，LPS诱导的IUGR不会改变成年期的代谢表型。
It is increasingly recognized that intra-uterine growth restriction (IUGR) is associated with an increased risk of metabolic disorders in late life. Previous studies showed that mice exposed to LPS in late gestation induced fetal IUGR. The present study investigated the effects of maternal LPS exposure during pregnancy on metabolic phenotypes in female adult offspring. Pregnant mice were intraperitoneally injected with LPS (50 µg/kg) daily from gestational day (GD)15 to GD17. After lactation, female pups were fed with standard-chow diets (SD) or high-fat diets (HFD). Glucose tolerance test (GTT) and insulin tolerance test (ITT) were assessed 8 and 12 weeks after diet intervention. Hepatic triglyceride content was examined 12 weeks after diet intervention. As expected, maternal LPS exposure during pregnancy resulted in fetal IUGR. Although there was an increasing trend on fat mass in female offspring whose dams were exposed to LPS during pregnancy, maternal LPS exposure during pregnancy did not elevate the levels of fasting blood glucose and serum insulin and hepatic triglyceride content in female adult offspring. Moreover, maternal LPS exposure during pregnancy did not alter insulin sensitivity in adipose tissue and liver in female adult offspring. Further analysis showed that maternal LPS exposure during pregnancy did not exacerbate HFD-induced glucose tolerance and insulin resistance in female adult offspring. In addition, maternal LPS exposure during pregnancy did not aggravate HFD-induced elevation of hepatic triglyceride content in female adult offspring. In conclusion, LPS-induced IUGR does not alter metabolic phenotypes in adulthood.