Publication | Open Access
Effects of Maternal LPS Exposure during Pregnancy on Metabolic Phenotypes in Female Offspring
24
Citations
45
References
2014
Year
NutritionMetabolic DisorderFetal HealthHigh-risk PregnancyObesityMetabolic SyndromeFetal Developmental ProgrammingMetabolic PhenotypesIntra-uterine Growth RestrictionMaternal NutritionPublic HealthMaternal Cardiovascular OutcomeClinical NutritionMaternal HealthGestational DiabetesDevelopmental EndocrinologyMaternal-fetal MedicineEndocrinologyMetabolic HealthPregnancy NutritionPlacental FunctionMaternal Lps ExposurePhysiologyDiabetesGlucose Tolerance TestFemale OffspringPregnancyLate GestationMetabolismMedicineWomen's Health
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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