Maternal body mass index and placental weight: a role for fetal insulin, maternal insulin and leptin.

PURPOSE: Placental weight (PW) has been found to mediate the main effect of maternal BMI on fetal size. Still, the BMI-PW association is poorly understood. Therefore, we aimed to explore potential explanatory variables, including gestational weight gain (GWG), early- and late-pregnancy circulating levels of maternal glucose, insulin, leptin, adiponectin, triglycerides, LDL-C, and HDL-C, and fetal insulin. METHODS: We included two studies of pregnant women from Oslo University Hospital, Norway: the prospective STORK (n = 263) and the cross-sectional 4-vessel method study (4-vessel; n = 165). We used multiple linear regression for data analyses. A non-linear BMI-PW association was observed, which leveled off from BMI25. Therefore, BMI <25 and ≥25 were analyzed separately (n = 170/122 and 93/43 for STORK/4-vessel). Confounding variables included maternal age, parity, and gestational age. RESULTS: PW increased significantly per kg m-2 only among BMI <25 (univariate model's std.ß[p] = 0.233 [0.002] vs. 0.074[0.48]/0.296[0.001] vs. -0.030[0.85] for BMI <25 vs. ≥25 in STORK/4-vessel). Maternal early- but not late-pregnancy insulin and term fetal insulin were associated with PW. The estimated effect of early pregnancy insulin was similar between the BMI groups but statistically significant only among BMI <25 (std.ß[p] = 0.182[0.016] vs. 0.203[0.07] for BMI <25 vs. ≥25). Late pregnancy leptin was inversely associated with PW with a 1.3/1.7-fold greater effect among BMI ≥25 than BMI <25 in the STORK/4-vessel. CONCLUSIONS: The BMI-PW association was non-linear: an association was observed for BMI <25 but not for BMI ≥25. Leptin may be involved in the non-linear association through a placental-adipose tissue interplay. Maternal early pregnancy insulin and fetal insulin at term were associated with PW.

PP071. suPAR levels in normal- and preeclamptic pregnancies.

INTRODUCTION: Preeclampsia (PE) has been considered to be a maternal inflammatory response to pregnancy and may be hazardous for mother and child. Soluble urokinase Plasminogen Activator receptor (suPAR) is a non-specific marker that reflects overall systemic inflammation and immune activation. OBJECTIVES: We examined the levels of suPAR in first and third trimesters of normal- and preeclamptic pregnancies. METHODS: Two clinical studies were conducted. The first study included 43 women who subsequently developed PE and 86 control women not developing PE. Blood samples were collected during the first trimester. The two groups were matched with respect to gestational age. In the second study, 13 cases of PE and 8 controls were enrolled and blood samples were collected during the third trimester. Serum suPAR were analyzed by the commercially availably suPARnostic® assay kit (ELISA, Virogates, Copenhagen, Denmark). RESULTS: There were no significant differences in first trimester suPAR level between women who subsequently developed PE and those who completed a normal pregnancy (4.5 [3.7-5.4] ng/mL versus 4.3 [3.8-5.0] ng/mL, p=0.49, median [interquartile range]). In the third trimester, suPAR levels were significantly elevated in the preeclamptic group compared to the control group (2.5 [2.2-3.5] ng/mL versus 1.9 [1.5-2.1] ng/mL, p=0.008). After adjustment for gestational age (38.6 (0.7) and 31 (3.1) weeks in the control- and the PE-group respectively, p<0.001, mean (SD)), the group difference did not remain statistically significant (p=0.064). CONCLUSION: suPAR is not a suitable marker for detecting the systemic maternal inflammatory response in women with established PE nor a useful pre-clinical marker of the disorder. The observation of the higher suPAR level in first trimester of pregnancy compared to third trimester suPAR level alludes to a possible physiological function that needs to be clarified.

Uteroplacental arterio-venous difference in soluble VEGFR-1 (sFlt-1), but not in soluble endoglin concentrations in preeclampsia.

The aim was to determine plasma levels of sFlt-1 and sEng on the arterial and venous side of the uteroplacental circulation in preeclamptic patients and healthy controls. Preeclamptic patients had higher arterial concentrations than controls of sFlt-1 (17,450 vs. 5055 pg/ml, p = 0.003) and sEng (68.7 vs. 28.7 ng/ml, p = 0.003). In the preclampsia group sFlt-1 was higher in the uterine vein than in the radial artery (22,450 vs. 17,450 pg/ml, p = 0.005). We found no gradient for sEng. Our results support the hypothesis that excess sFlt-1 at least partly originates in placenta, while excess sEng appears to have a different origin.