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Placental lactogen (A) and prolactin concentrations (B) in maternal plasma samples collected from pregnant women at 20 weeks of gestation who went on to have babies of normal birth weight (control, n = 40) or small for gestational age (SGA, <10th centile, n = 40). One sample was removed from the control placental lactogen group as it was tested to be an outlier. Placental lactogen, P = 0.3868 (one-tailed Mann-Whitney nonparametric test as data were not normally distributed (SGA group P < 0.05 D'Agostino and Pearson normality test)). Human prolactin, P = 0.0582 (Student's one-tailed t-test). Data shown as mean ± s.d.
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Prolactin and placental lactogens increase during pregnancy and are involved with many aspects of maternal metabolic adaptation to pregnancy, likely to impact on fetal growth. The aim of this study was to determine whether maternal plasma prolactin or placental lactogen concentrations at 20 weeks of gestation were associated with later birth of sma...
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Context 1
... significant differences were detected in maternal plasma placental lactogen or prolactin concentrations between the uncomplicated pregnancy and SGA groups (placental lactogen: P = 0.7736 two-tailed Mann-Whitney tests, prolactin: P = 0.1164 two-tailed t-test) (Fig. 1). When specifically investigating the hypothesis that low lactogenic hormone activity would be associated with SGA pregnancies, there was no statistically significant difference in prolactin concentrations in pregnancies that went on to have a SGA infant compared to those with uncomplicated pregnancies (P = 0.058). To determine whether ...
Citations
... Consistent with our findings, in humans, there is a down-regulation of the growth hormone/chorionic somatomammotropin (hGH/CSH) cluster in the SGA placenta (67). Moreover, other work has shown that mothers carrying SGA male fetuses display lower concentrations of prolactin in their circulation when compared to women carrying AGA male fetuses (68). In our mouse model, the expression of Cyp17a1 was lower in the SGA versus AGA fetuses. ...
Conditions such as small for gestational age (SGA), which is defined as birthweight less than 10th percentile for gestational age can predispose to neurodevelopmental abnormalities compared to babies with normal birthweight. Fetal growth and birthweight depend on placental function, as this organ transports substrates to the developing fetus and it acts as a source of endocrine factors, including steroids and prolactins that are required for fetal development and pregnancy maintenance. To advance our knowledge on the aetiology of fetal growth disorders, the vast majority of the research has been focused on studying the transport function of the placenta, leaving practically unexplored the contribution of placental hormones in the regulation of fetal growth. Here, using mice and natural variability in fetal growth within the litter, we compared fetuses that fell on or below the 10th percentile (classified as SGA) with those that had adequate weight for their gestational age (AGA). In particular, we compared placental endocrine metabolism and hormone production, as well as fetal brain weight and expression of developmental, growth and metabolic genes between SGA and AGA fetuses. We found that compared to AGA fetuses, SGA fetuses had lower placental efficiency and reduced capacity for placental production of hormones (e.g. steroidogenic gene Cyp17a1, prolactin Prl3a1, and pregnancy-specific glycoproteins Psg21). Brain weight was reduced in SGA fetuses, although this was proportional to the reduction in overall fetal size. The expression of glucose transporter 3 (Slc2a3) was reduced despite the abundance of AKT, FOXO and ERK proteins were similar. Developmental (Sv2b and Gabrg1) and microglia genes (Ier3), as well as the pregnancy-specific glycoprotein receptor (Cd9) were lower in the brain of SGA versus AGA fetuses. In this mouse model of SGA, our results therefore demonstrate that placental endocrine dysfunction is associated with changes in fetal growth and fetal brain development.
