Relationships between placental GH concentration and maternal smoking, newborn gender, and maternal leptin: Possible implications for birth weight

The control of fetal growth depends on multiple hormones, including both IG F-I and placental GH (PGH) in the mother, and IGF-I rather than pituitary G H (pitGH) in the fetus. Leptin, which is produced by adipocytes and synciti otrophoblast cells, has also been thought to influence fetal growth by an a s 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 on set of labor and cord blood immediately after birth in their 87 healthy ful l-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) mug /liter, P < 0.01]. Cord blood IGF-I was lower in neonates from smoking moth ers (90 +/- 44 vs. 135 +/- 65 <mu>g/liter, mean +/- SD, P < 0.01), consiste nt 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 m aternal smoking category (P < 0.05 for all comparisons). Multiple regression analyses identified maternal leptin as a negative predi ctor of PGH (P < 0.05) and newborn leptin as a positive predictor of newbor n 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 rema ins to be studied. The relationships between maternal leptin and PGH and be tween cord blood leptin and IGF-I are consistent with the hypothesis that l eptin could contribute to the control of fetal growth.