Effects of maternal LPS exposure during pregnancy on metabolic phenotypes in female offspring.

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 expos...

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Main Authors: Xiao-Jing Liu, Bi-Wei Wang, Mei Zhao, Cheng Zhang, Yuan-Hua Chen, Chun-Qiu Hu, Hui Zhao, Hua Wang, Xi Chen, Fang-Biao Tao, De-Xiang Xu
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4257726?pdf=render
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author Xiao-Jing Liu
Bi-Wei Wang
Mei Zhao
Cheng Zhang
Yuan-Hua Chen
Chun-Qiu Hu
Hui Zhao
Hua Wang
Xi Chen
Fang-Biao Tao
De-Xiang Xu
author_facet Xiao-Jing Liu
Bi-Wei Wang
Mei Zhao
Cheng Zhang
Yuan-Hua Chen
Chun-Qiu Hu
Hui Zhao
Hua Wang
Xi Chen
Fang-Biao Tao
De-Xiang Xu
author_sort Xiao-Jing Liu
collection DOAJ
description 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.
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spelling doaj.art-f348941e710547319c4156e5e3c59d052022-12-22T01:34:57ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-01912e11478010.1371/journal.pone.0114780Effects of maternal LPS exposure during pregnancy on metabolic phenotypes in female offspring.Xiao-Jing LiuBi-Wei WangMei ZhaoCheng ZhangYuan-Hua ChenChun-Qiu HuHui ZhaoHua WangXi ChenFang-Biao TaoDe-Xiang XuIt 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.http://europepmc.org/articles/PMC4257726?pdf=render
spellingShingle Xiao-Jing Liu
Bi-Wei Wang
Mei Zhao
Cheng Zhang
Yuan-Hua Chen
Chun-Qiu Hu
Hui Zhao
Hua Wang
Xi Chen
Fang-Biao Tao
De-Xiang Xu
Effects of maternal LPS exposure during pregnancy on metabolic phenotypes in female offspring.
PLoS ONE
title Effects of maternal LPS exposure during pregnancy on metabolic phenotypes in female offspring.
title_full Effects of maternal LPS exposure during pregnancy on metabolic phenotypes in female offspring.
title_fullStr Effects of maternal LPS exposure during pregnancy on metabolic phenotypes in female offspring.
title_full_unstemmed Effects of maternal LPS exposure during pregnancy on metabolic phenotypes in female offspring.
title_short Effects of maternal LPS exposure during pregnancy on metabolic phenotypes in female offspring.
title_sort effects of maternal lps exposure during pregnancy on metabolic phenotypes in female offspring
url http://europepmc.org/articles/PMC4257726?pdf=render
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