To evaluate the effects of maternal pre-pregnancy body mass index (pre-BMI) and gestational weight gain (GWG) on neonatal birth weight (NBW) in the population of Chinese healthy pregnant women, attempting to guide weight control in pregnancy. A retrospective cohort study of 3772 Chinese women was conducted. The population was stratified by maternal pre-BMI categories as underweight (<18.5 kg/m), normal weight (18.5-23.9 kg/m), overweight (24.0-27.9 kg/m), and obesity (≥28.0 kg/m). The NBW differences were tested among the four groups, and then deeper associations among maternal pre-BMI, GWG, and NBW were investigated by multivariate analysis. NBW increased significantly with the increase of maternal pre-BMI level (P<0.05), except overweight to obesity (P>0.05). The multivariate analysis showed that both pre-BMI and GWG were positively correlated with NBW (P<0.05). Compared with normal pre-BMI, underweight predicted an increased odds ratio of small-for-gestational-age (SGA) and decreased odds ratio for macrosomia and large-for-gestational-age (LGA), and the results were opposite for overweight. With the increase of GWG, the risk of SGA decreased and the risks of macrosomia and LGA increased. In addition, in different pre-BMI categories, the effects of weight gain in the first trimester on NBW were different (P<0.05). NBW is positively affected by both maternal pre-BMI and GWG, extreme pre-BMI and GWG are both associated with increased risks of abnormal birth weight, and maternal pre-BMI may modify the effect of weight gain in each trimester on NBW. A valid GWG guideline for Chinese women is an urgent requirement, whereas existing recommendations seem to be not very suitable for the Chinese.

Aims: To clarify the role of fatty acid-binding protein 4 (FABP4) of endometrial epithelial cell in the establishment and maintenance of pregnancy and the involvement in the pathogenesis of pregnancy loss. Methods: The expression of FABP4 and uterine receptive factor (LIF, Integrin-β3 and Claudin 4) was determined by Western blotting or quantitative PCR. FABP4 siRNA was used to silence FABP4 while FABP4 inhibitor was used to inhibit the function of FABP4 in endometrial epithelial cell. ICR mice were raised to evaluate the effect of FABP4 silence or inhibition on embryo implantation in vivo after FABP4 siRNA mixture or inhibitor was injected into uterus, and an embryonic adhesion system using trophoblast spheroids mimicking embryos was set up to assess the effect of FABP4 silence or inhibition on embryonic adhesion onto endometrial cell in vitro. Results: The expression of FABP4 mRNA was significantly decreased in the deciduas of women with pregnancy loss compared with that of women with normal pregnancy. FABP4 siRNA significantly reduced the number of embryos implanted and FABP4 expression in ICR mice. FABP4 inhibition also significantly decreased the number of embryos implanted. Either silence or inhibition of FABP4 in endometrial epithelial cell abolished the expression of uterine receptive factors induced by the combination of estrogen and progesterone-induced, and reduced the number of trophoblast spheroids adhered onto endometrial cell. Conclusions: FABP4 regulates embryo implantation via altering uterine receptivity and decreased expression of FABP4 in endometrium may be linked with pregnancy loss, indicating FABP4 has biological role in the establishment and maintenance of pregnancy and subsequently is involved in pathogenesis of pregnancy loss.

Background: This study aimed to clarify the change of the expression of placenta-specific 1 (PLAC1) in the placenta of preeclamptic women and to explore the regulatory effects on thophoblast by PLAC1.Methods: Nineteen women with preeclampsia and 19 with normal pregnancies were recruited, and then we determined the expression of PLAC1 by immunohistochemistry (IHC) and Western blotting. To observe the effect of hypoxia on the expression of PLAC1, trophoblasts were cultured at the normoxia or hypoxia condition. Small interference of ribonucleic acid (siRNA) was used to silence PLAC1. The proliferation, migration and invasion of trophoblasts were evaluated with cell counting kit-8 and transwell analysis, and the apoptosis of trophoblast was evaluated by flow cytometry with FITC and PI staining.Results: Placental PLAC1 expression was significantly decreased in severe preeclampsia compared with control (P < .001). The expression of PLAC1 in trophoblasts was significantly decreased after treated with low oxygen concentration (P = .018). PLAC1 siRNA significantly inhibited the proliferation (P < .001), the migration (P < .001) and invasion (P < .001) of trophoblasts, but increased the apoptosis (P = .004 for Swan-71; P = .031 for Jar).Conclusions: The expression of PLAC1 was declined in preeclampsia and this inhibited the function of trophoblast, suggesting PLAC1 may play a role in the development of preeclampsia.

BackgroundThe lipoprotein subfraction particle profile can be used to improve clinical assessments of cardiovascular disease risk and contribute to early detection of atherogenic dyslipidemia. Lipid alterations in gestational diabetes have been extensively studied, but the results have been inconsistent. Here, we investigated serum lipoprotein subfraction particle levels and their association with glucose metabolic status in pregnancy.MethodsTwenty-eight pregnant women with gestational diabetes and 56 pregnant women with normal glucose tolerance matched for body mass index were enrolled in this study. We assessed fasting serum lipid concentrations and lipoprotein subfraction particle levels in participants between 24 and 28 weeks of gestation.ResultsThe level of low-density lipoprotein (LDL) cholesterol was significantly lower in women with gestational diabetes than in those with normal glucose tolerance, but the triglyceride and high-density lipoprotein (HDL) cholesterol levels of the two groups were similar. Lipoprotein particle analysis showed that very-low-density lipoprotein (VLDL) particle number and the small dense LDL particle/large buoyant LDL particle (sdLDL-P/lbLDL-P) ratio were significantly higher in women with gestational diabetes than in those with normal glucose tolerance (P = 0.013 and P = 0.015, respectively). In multivariate analysis, fasting glucose was independently and positively associated with sdLDL-P/lbLDL-P ratio even after adjustment for maternal age, gestational weight gain, BMI and LDL cholesterol (standardized Beta = 0.214, P = 0.029).ConclusionsThe sdLDL-P/lbLDL-P ratio is higher in GDM compared with non-diabetic pregnant women, and positively and independently associated with fasting glucose in pregnant women.