Relationships between Placental GH Concentration and Maternal Smoking, Newborn Gender, and Maternal Leptin: Possible Implications for Birth Weight

Abstract

The control of fetal growth depends on multiple hormones, including both IGF-I and placental GH (PGH) in the mother, and IGF-I rather than pituitary GH (pitGH) in the fetus. Leptin, which is produced by adipocytes and syncitiotrophoblast cells, has also been thought to influence fetal growth by an as yet unknown mechanism. This study assessed the relationships between the GH-IGF-I axis in mothers and newborns, and maternal smoking, neonate gender, and maternal and fetal leptin. We collected blood in 87 mothers at the onset of labor and cord blood immediately after birth in their 87 healthy full-term newborns. GH concentrations were log(10) transformed, and data were expressed as the geometric mean (-1, +1 tolerance factor). PGH was lower in the 30 smoking mothers, as compared with the 57 nonsmoking mothers [18.2 (11.5; 28.6) vs. 27.0 (15.1; 48.2) microg/liter, P < 0.01]. Cord blood IGF-I was lower in neonates from smoking mothers (90 +/- 44 vs. 135 +/- 65 microg/liter, mean +/- SD, P < 0.01), consistent with their lower birth weight percentile (P < 0.01). A gender effect was observed for PGH, which was higher when the newborn was female, and for newborn pitGH and newborn leptin, which were, respectively, lower and higher in females, even after adjustment for birth weight and maternal smoking category (P < 0.05 for all comparisons). Multiple regression analyses identified maternal leptin as a negative predictor of PGH (P < 0.05) and newborn leptin as a positive predictor of newborn IGF-I (P < 0.05). Maternal smoking is associated to decreased maternal PGH and cord blood IGF-I concentrations. A sexual dimorphism for PGH, newborn pitGH, and newborn leptin exists at the time of birth, but its physiological significance remains to be studied. The relationships between maternal leptin and PGH and between cord blood leptin and IGF-I are consistent with the hypothesis that leptin could contribute to the control of fetal growth.

Human placental growth hormone in normal and abnormal fetal growth

“…A positive correlation between PGH and fetal and neonatal weight has been demonstrated (46–48). PGH levels decline during an oral glucose tolerance test in women with gestational diabetes (4).…”

“…This is a pregnancy-specific hormone that along with other hormones coordinates trophoblast invasion (8), fetal growth (3,46,51) and maternal adaptation to pregnancy (9,10). The somatotrophic, lactogenic and lipolytic action of PGH resembles that of pituitary GH.…”

Leptin levels in cord blood and anthropometric measures at birth: a systematic review and meta‐analysis

“…Minor disagreements, for example on the selection of the most appropriate effect estimates, were also limited. The study design included seven birth cohorts, 21,[31][32][33]46,52,58 four pregnancy cohorts, 30,39,54,63 32 cross-sectional 20,22,23,[25][26][27][28][29][34][35][36][37][38][40][41][42][43][44][45][47][48][49][50][51]53,[55][56][57][59][60][61][62] and one case-control study. 24 All of these studies were essentially cross-sectional with respect to the key outcomes.…”

“…The average sample size of these 44 studies was 119.3 neonates (range 22-585). Considering the assay used for the measurement of cord leptin, 35 studies employed radioimmunoassay (RIA), [21][22][23][24][28][29][30][31][34][35][36][37][38][39][40][41][42][43][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61]63 while seven studies used ELISA 20,26,27,32,33,44,62 and two others used a two-site immunoradiometric assay (IRMA). 25,45 In six studies, 21,35,38,50,52,63 log leptin wa...…”

Comparison of maternal ghrelin and leptin in healthy mothers and mothers with Type 1 diabetes

“…Although infants of T1DM mothers have lower ghrelin levels [7], ghrelin may be one of the determinants of abnormal fetal growth. Leptin, which regulates energy homeostasis [8], may also contribute to the control of fetal growth and is associated with placental GH [9]. Much higher free leptin levels are found in human obesity, suggesting that leptin binding proteins may become saturated with obesity [10], particularly the soluble form of the leptin receptor (sOB-R), a binding protein for leptin that decreases with obesity [10,11].…”