Intrauterine growth restriction (IUGR) is associated with increased leptin synthesis and binding capability in neonates

P>Objective Animal studies suggest pathological foetal programming of hypothalamic circuits regulating food intake in the setting of leptin deficiency and intrauterine growth restriction (IUGR). We aimed to compare placental leptin synthesis and leptin-binding capability in venous cord blood between IUGR newborns and neonates born appropriate for gestational age (AGA). Design Prospective controlled multicentre study. Patients Twenty-one ultrasound-proven IUGR and 33 AGA neonates. Measurements The concentration of leptin and soluble leptin receptor (sOB-R) in venous cord blood at birth was determined. Moreover, placental gene and protein expression of leptin and placental mRNA expression of functional and total leptin receptor isoforms were measured. Results Whereas log-leptin concentration in venous cord blood did not differ between IUGR and AGA newborns, the concentration of log-sOB-R was elevated in IUGR neonates (pconfounder adjusted = 0 center dot 009). Placental leptin protein synthesis as well as leptin mRNA was significantly higher in IUGR than in AGA infants (log-transformed, relative gene expression, pconfounder adjusted = 0 center dot 004). Analysis of gene expression of functional and total leptin receptor isoforms did not show any difference between both groups. Conclusions Leptin-binding capability in venous cord blood is increased in IUGR newborns. Thus, via foetal programming, reduced biologically active leptin levels might contribute to a perturbed regulation of appetite.