title: Placental 11beta-HSD2 gene expression at birth is inversely correlated with growth velocity in the first year of life after intrauterine growth restriction.
abstract: Intrauterine growth restriction (IUGR) is associated with an increased risk for short stature and diseases in adulthood thought to be inflicted by fetal programming. We hypothesized that placental endocrine systems involved in perinatal growth might also play a role in postnatal growth after IUGR. In a prospective controlled multicenter study, placental gene expression of IGF-binding protein-1 (IGFBP-1), leptin and 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) were measured in 14 IUGR infants and 15 children born appropriate for gestational age (AGA) proven by serial ultrasound examinations. Postnatally, IUGR infants experienced a significantly higher growth velocity than AGA neonates (at 1 y: p = 0.001). Gene expression of 11beta-HSD2 at birth correlated positively with birth length (r = 0.55, p = 0.04) and inversely with growth velocity in the first year of life (r = -0.69, p = 0.01) in the IUGR, but not in the AGA group. There was no correlation between gene expression of placental IGFBP-1, leptin and birth weight, length and growth velocity during the first year of life. AGA infants showed significantly higher concentrations of cortisone in venous cord blood after birth (p = 0.02) as a surrogate of a higher 11beta-HSD2 activity in the fetoplacental unit. In conclusion, placental 11beta-HSD2 gene expression might predict postnatal growth in IUGR.
authors.affiliation: Department of Paediatrics and Adolescent Medicine, University of Erlangen-Nuremberg, Erlangen, Germany.
authors.forename: Anja
authors.initials: A
authors.lastname: Tzschoppe
authors.forename: Ellen
authors.initials: E
authors.lastname: Struwe
authors.forename: Holger
authors.initials: H
authors.lastname: Blessing
authors.forename: Fabian
authors.initials: F
authors.lastname: Fahlbusch
authors.forename: Gisela
authors.initials: G
authors.lastname: Liebhaber
authors.forename: Helmuth G
authors.initials: HG
authors.lastname: Dörr
authors.forename: Manfred
authors.initials: M
authors.lastname: Rauh
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Rascher
authors.forename: Tamme W
authors.initials: TW
authors.lastname: Goecke
authors.forename: Ralf L
authors.initials: RL
authors.lastname: Schild
authors.forename: Ekkehard
authors.initials: E
authors.lastname: Schleussner
authors.forename: Cerrie
authors.initials: C
authors.lastname: Scheler
authors.forename: Axel
authors.initials: A
authors.lastname: Hübler
authors.forename: Peter
authors.initials: P
authors.lastname: Dahlem
authors.forename: Jörg
authors.initials: J
authors.lastname: Dötsch
mesh_terms: D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2 / Q000235:genetics / Q000378:metabolism; D000886:Anthropometry; D001724:Birth Weight / Q000235:genetics; D005260:Female; D047109:Fetal Development / Q000235:genetics; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D005865:Gestational Age; D006801:Humans; D007223:Infant; D018970:Insulin-Like Growth Factor Binding Protein 1 / Q000235:genetics / Q000378:metabolism; D020738:Leptin / Q000235:genetics / Q000378:metabolism; D008297:Male; D010920:Placenta / Q000201:enzymology* / Q000502:physiology; D011247:Pregnancy; D011446:Prospective Studies
chemical_list: C032231:IGFBP1 protein, human; D018970:Insulin-Like Growth Factor Binding Protein 1; D020738:Leptin; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2