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.