Maternal Serum Leptin Concentrations Do Not Correlate With Cord Blood Leptin Concentrations in Normal Pregnancy

Objective:To determine whether there is a difference in maternal leptin concentration and cord blood concentration, consistent with the hypothesis of a noncommunicating, two-compartement model of fetoplacental leptin regulation.Methods:Blood samples were collected from 139 women, identified as having an uncomplicated pregnancy, from an antecubital vein at delivery. Cord blood samples were taken from the umbilical vein. Leptin was measured by radioimmunoassay, and its relationship to fetal and maternal anthropometrics was assessed by Spearman correlation. Differences in maternal and cord blood leptin levels between male and female infants were tested twith the Mann-Whitney U test. Maternal and cord blood leptin were compared by the Wilcoxon signed rank test. The outcome measures were maternal and cord blood leptin at delivery, fetal birth weight, length, weight/length ratio, and ponderal index, maternal prepregnancy body mass index, pregnancy weight gain, relative weight gain, and body mass index at delivery.Results:No correlations were found between maternal and cord blood leptin concentrations. Fetal leptin level correlated with birth weight (ρ = 0.665; p < .0001), length (ρ = 0.490; P < .0001), ponderal index (ρ = 0.260; P = .002), and weight/length ratio (ρ = 0.625; P < .0001). Median leptin concentrations were higher in female (9.3 ng/mL, range 1.5-34.4 ng/mL) than in male (8.2 ng/mL, range 1.6-38.3 ng/mL) neonates, but this difference was statistically not significant. Logistic regression analysis showed a significant influence on umbilical venous leptin concentration for birth weight (P < .0001) but not for gender. Maternal leptin concentrations were significantly higher than cord leptin concentrations (P < .0005 for the male and female neonates and the entire group).Conclusion:There was no correlation between maternal and cord leptin, whiich supports the hypothesis of a noncommunicating, two-compartment model of fetoplacental leptin regulation.