Effect of Maternal Obesity on Fetal Growth and Expression of Placental Fatty Acid Transporters.

OBJECTIVE: To explore the effects of maternal high-fat (HF) diet-induced obesity on fetal growth and the expression of placental nutrient transporters. METHODS: Maternal obesity was established in rats by 8 weeks of pre-pregnancy fed HF diet, while rats in the control group were fed normal (CON) diet. Diet-induced obesity (DIO) rats and diet-induced obesity-resistant (DIR) rats were selected according to body weight gain over this period. After copulation, the CON rats were divided into two groups: switched to HF diet (CON-HF group) or maintained on the CON diet (CON-CON group). The DIO rats and DIR rats were maintained on the HF diet throughout pregnancy. Pregnant rats were euthanized at day 21 gestation, fetal and placental weights were recorded, and placental tissue was collected. Reverse transcription-polymerase chain reaction was used to determine mRNA expression of placental nutrient transporters. Protein expression was determined by Western blot. RESULTS: Average fetal weight of DIO dams was reduced by 6.9%, and the placentas of CON-HF and DIO dams were significantly heavier than the placentas of CON-CON and DIR dams at day 21 of gestation (p<0.05). The fetal/placental weight ratio of DIO dams was significantly reduced compared with the fetal/placental weight ratio of CON-CON dams (p<0.05). The mRNA expression of GLUT-1 and SNAT-2 were not significantly different between groups. The mRNA and protein expression levels of CD36, FATP-1, and FATP-4 in DIO dams were decreased significantly (p<0.05). CONCLUSION: Maternal obesity induced by a HF diet led to intrauterine growth retardation and down-regulated the expression of placental fatty acid transporters.

The Relationship between Maternal Gestational Impaired Glucose Tolerance and Risk of Large-for-Gestational-Age Infant: A Meta-Analysis of 14 Studies.

OBJECTIVE: To explore, by conducting a meta-analysis, whether gestational impaired glucose tolerance (IGT) is an independent predictor of neonatal large for gestational age (LGA) or not. METHODS: Medline, Embase, and Cochrane Library databases were searched to identify published epidemiological studies (cohort and case-control studies) investigating the association between gestational IGT and neonatal LGA. Calculations of pooled estimates were conducted in random-effect models or fixed-effects models. Heterogeneity was tested by using chi-square test and I2 statistics. Egger's test (linear regression method) and Begg's test (rank correlation method) were used to assess potential publication bias. RESULTS: Fourteen observational studies were included in the meta-analysis. The overall risk for the effect of IGT on LGA was 2.09 (1.56, 2.78). Stratified analyses showed no differences regarding different geographic regions or the analysis of overall adjusted odds ratios. No evidence of publication bias was observed in either Egger's test or Begg's test results. CONCLUSION: Gestational IGT is an independent predictor of neonatal LGA.

Weight gain in pregnancy, maternal age and gestational age in relation to fetal macrosomia.

To investigate the possible risk factors related to macrosomia. Pregnant women and their newborns (n = 1041) were recruited from a cohort study in Maternal and Child Care Center of Hefei from January 2011 to July 2012. Questionnaires were applied to collect the demographic data besides the medical records. Detailed health records of the entire pregnancy were obtained using retrospective study. Meanwhile the data of neonatal outcomes was prospectively tracked. Associations between exposure risk factors and macrosomia were analyzed using Pearson's chi squared test. Logistic regression models were used to assess the independent association between these potential predictors and macrosomia. The incidence of macrosomia of this cohort was 11.24% of which male: female = 2.55:1. Male incidence (8.07%) of macrosomia was higher than female (3.17%), p < 0.001. Body mass index (BMI) before pregnancy (pre-BMI), maternal height, parity were not independently associated with macrosomia; multiple logistic regression analysis indicated that macrosomia was mainly independently associated with weight gain in pregnancy (OR=1.14, 95% CI [1.10-1.19]), maternal age (OR = 1.09, 95% CI [1.03-1.15]) and gestational age (OR = 1.62, 95% CI [1.31-1.99]), respectively. Our findings indicate that weight gain in pregnancy, maternal age and gestational age should be considered as independent risk factors for macrosomia.