Objective: Infants born from overweight and obese mothers with glucose-controlled gestational diabetes (GDM) tend to be large-for-gestational age (LGA). It is hypothesized that this is due to an excessive rise in maternal triglyceride levels. Methods: Two-hundred and seventy nine singleton GDM pregnancies were divided into three groups according to prepregnancy BMI: normal weight (BMI 5 20-24.9; n 5 128), overweight (BMI 5 25-29.9; n 5 105), and obese (BMI 30; n 5 46). Individual z-scores (ZS) of maternal triglycerides and of newborn weight (NWZS) were calculated as deviations from published 50th percentiles. Mean z-scores (MZS) were the average of triglyceride ZSs. MZS of triglycerides, HbA1c and NWZS were compared. Variables are expressed as mean 6 SD. Results: In the three groups respectively: LGA (%) 5 10.1%, 19.0% and 30.4% (P 5 0.015). Birth weight (g) 5 3274.2 6 501.3, 3342.4 6 620.2 and 3366.36644.7 (R SPEARMAN 5 0.111, P 5 0.027). HbA1c (%) 5 5.2 6 0.39, 5.3 6 0.50 and 5.4 6 0.47 (P 5 NS). Triglyceride MZS 5 1.20 6 1.13, 1.52 6 1.37 and 1.62 6 1.42 (R SPEARMAN 5 0.116, P 5 0.024). Correlations between triglyceride MZS and NWZS were, respectively: r 5 0.12 (P 5 NS), r 5 0.42 (P <0.001), and r 5 0.47 (P < 0.001). Conclusions: In overweight and obese GDM mothers, maternal triglycerides are partially responsible for LGA infants despite good maternal glucose control during pregnancy.

Women age as a risk factor for maternal, fetal, neonatal and infant mortality (Rev Med Chile 2014; 142: 168-174)

Abstractj og_1681 208..214Aim: Good glycemic control in gestational diabetes mellitus (GDM) seems not to be enough to prevent macrosomia (large-for-gestational-age newborns). In GDM pregnancies we studied the effects of glycemic control (as glycosylated hemoglobin [HbA1c]), pre-pregnancy body mass index (PP-BMI) and gestational weight gain per week (GWG-W) on the frequency of macrosomia. Methods: We studied 251 GDM pregnancies, divided into two groups: PP-BMI < 25.0 kg/m 2 (the nonoverweight group; n = 125), and PP-BMI Ն 25.0 kg/m 2 (the overweight group; n = 126). A newborn weight Z-score > 1.28 was considered large-for-gestational-age. Statistical analysis was carried out using the Student's t-test and c 2 -test, receiver-operator characteristic curves and linear and binary logistic regressions. Results: Prevalence of macrosomia was 14.9% among GDM (n = 202/251, 88.4%) with good glycemic control (mean HbA1c < 6.0%), and 28.1% in those with mean HbA1c Ն 6.0% (n = 49/251, P < 0.025). Macrosomia rates were 10.4% in the non-overweight group and 24.6% in the overweight group (P = 0.00308), notwithstanding both having similar mean HbA1c (5.48 Ϯ 0.065 and 5.65 Ϯ 0.079%, P = 0.269), and similar GWG-W (0.292 Ϯ 0.017 and 0.240 Ϯ 0.021 kg/week, P = 0.077). Binary logistic regressions showed that PP-BMI (P = 0.012) and mean HbA1c (P = 0.048), but not GWG-W (P = 0.477), explained macrosomia. Conclusions: Good glycemic control in GDM patients was not enough to reduce macrosomia to acceptable limits (<10% of newborns). PP-BMI and mean HbA1c (but not GWG-W) were significant predictors of macrosomia. Thus, without ceasing in our efforts to improve glycemic control during GDM pregnancies, patients with overweight/obesity need to be treated prior to becoming pregnant.

We conclude that human fetal membranes release one or more factors that inhibit oxytocin-induced myometrial contractility. We suggest this factor (or factors) acts mainly by opening myometrial BK(Ca). The findings further support our hypothesis that the fetal membranes release a factor (or factors) that is central to myometrial quiescence and its premature loss leads to preterm delivery.