title: 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.
authors.affiliation: Department of Pediatrics, University Hospital, 4 rue Larrey, 49000 Angers, France. recoutant@chu-angers.fr
authors.forename: R
authors.initials: R
authors.lastname: Coutant
authors.forename: F
authors.initials: F
authors.lastname: Boux de Casson
authors.forename: O
authors.initials: O
authors.lastname: Douay
authors.forename: E
authors.initials: E
authors.lastname: Mathieu
authors.forename: S
authors.initials: S
authors.lastname: Rouleau
authors.forename: F
authors.initials: F
authors.lastname: Beringue
authors.forename: P
authors.initials: P
authors.lastname: Gillard
authors.forename: J M
authors.initials: JM
authors.lastname: Limal
authors.forename: P
authors.initials: P
authors.lastname: Descamps
mesh_terms: D001724:Birth Weight; D005314:Embryonic and Fetal Development; D005260:Female; D019382:Human Growth Hormone / Q000032:analysis*; D006801:Humans; D007231:Infant, Newborn; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D020738:Leptin / Q000097:blood*; D008297:Male; D010920:Placenta / Q000737:chemistry*; D011247:Pregnancy; D012727:Sex Characteristics; D012907:Smoking / Q000097:blood*
chemical_list: D018972:Insulin-Like Growth Factor Binding Protein 3; D020738:Leptin; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I