Leptin production and release in the dually in vitro perfused human placenta

There is clear evidence that the placenta produces leptin. However, it is s till unclear to what extent leptin is released into the maternal and the fe tal circulation. The aim of our study was to determine placental leptin rel ease rates into these 2 compartments. In 10 term placentas, using dual in, vitro perfusion of an isolated cotyledon, concentrations of leptin, hCG, an d human placental lactogen (hPL) were determined in perfusates and in the t issue before and after perfusion. With perfusions lasting 270-840 min, tota l leptin production was 225 pg/g.min [median; interquartile range (IQR), 76 -334 pg/g.min]. The release into the fetal circulation was very low (median , 2.5; IQR, 1.1-5.9 pg/g.min) compared with the release into the maternal c irculation (median, 203; IQR, 79-373 pg/g.min) corresponding to 1.6% and 98 .4% of net release. Only 0.05% of hPL and hCG were released into the fetal circulation and 99.95% into the maternal circulation, confirming previous r esults. Release into the fetal circulation correlated significantly with re lease into the maternal circulation for leptin (r = 0.648; P < 0.05) and hP L (r = 0.721; P < 0.05). Furthermore, release of leptin into the fetal circ ulation was positively correlated with release of fetal hCG (r = 0.661; P < 0.05). Most of the leptin produced by the placenta is released into the maternal c irculation, but compared with other placental hormones (hCG and hPL), a con siderably higher proportion of leptin is released into the fetal circulatio n. These findings may at least partially explain the marked increase in mat ernal serum leptin levels in pregnancy. The rapid postnatal decrease in lep tin levels in both the mother and the neonate is also consistent with the c oncept of placental origin.