title: Leptin and adiponectin concentrations in intrauterine growth restricted and appropriate for gestational age fetuses, neonates, and their mothers.
abstract: OBJECTIVE
  Leptin and adiponectin are two adipocytokines that play a critical role in the control of energy balance and metabolism as well as in conditions, such as insulin resistance, inflammation, and the development of the metabolic syndrome in adult life. Leptin has been associated with asymmetric intrauterine growth restriction (IUGR). The aim of this study was to investigate the perinatal implication of leptin and adiponectin in IUGR. Design Leptin and adiponectin were measured in the plasma of 40 mothers, in the umbilical cord (UC) blood of their 20 appropriate for gestational age (AGA) and 20 IUGR singleton, full-term fetuses, and neonates on day 1 (d1) and day 4 (d4) of life postnatally.
  
  
  METHODS
  Serum leptin and adiponectin levels were measured by RIA. Serum cortisol levels were measured with an electrochemiluminescence immunoassay.
  
  
  RESULTS
  Leptin and adiponectin serum levels were higher and lower respectively in IUGR (mean+/-s.e.m., 32.5+/-3.8 and 5.4+/-0.9 mug/l respectively) compared with AGA (20.4+/-2.1 and 11.8+/-1.3 mug/l respectively) mothers (P<0.05), although body mass index did not differ between these two groups. Leptin levels positively correlated with adiponectin levels in the AGA (r=0.547, P<0.05) but not in the IUGR mothers. UC, d1, and d4 leptin and adiponectin levels did not differ between IUGR and AGA groups. UC were significantly higher than d1 leptin levels (P<0.05) in the IUGR group but not in the AGA group.
  
  
  CONCLUSIONS
  The increased UC leptin levels compared with d1 in IUGR fetuses might be directly and/or indirectly related to the subsequent development of insulin resistance in these neonates. This pathologic situation seems to be related to a specific profile of increased leptin and decreased adiponectin levels in IUGR mothers indicating a genetic predisposition for the development of insulin resistance.
authors.affiliation: Neonatal and Endocrine Unit, Second Department of Obstetrics and Gynecology, Athens University Medical School, 10682 Athens, Greece.
authors.forename: Marialena
authors.initials: M
authors.lastname: Kyriakakou
authors.forename: Ariadne
authors.initials: A
authors.lastname: Malamitsi-Puchner
authors.forename: Helen
authors.initials: H
authors.lastname: Militsi
authors.forename: Theodora
authors.initials: T
authors.lastname: Boutsikou
authors.forename: Alexandra
authors.initials: A
authors.lastname: Margeli
authors.forename: Demetrios
authors.initials: D
authors.lastname: Hassiakos
authors.forename: Christina
authors.initials: C
authors.lastname: Kanaka-Gantenbein
authors.forename: Ioannis
authors.initials: I
authors.lastname: Papassotiriou
authors.forename: George
authors.initials: G
authors.lastname: Mastorakos
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D000886:Anthropometry; D004734:Energy Metabolism / Q000502:physiology; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism*; D005333:Fetus / Q000378:metabolism; D005865:Gestational Age; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007231:Infant, Newborn; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism*
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D020738:Leptin; D006854:Hydrocortisone