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Leptin Production and Release in the Dually in VitroPerfused Human Placenta¹

Department of Neonatology, University Children’s Hospital (K.L., C.F.), D-17489 Greifswald, Germany; Department of Obstetrics and Gynecology, Insel Spital, University of Bern (A.M., R.S., H.S.), CH-3012 Bern, Switzerland; and Lilly Research Laboratories (W.F.B.), D-61350 Bad Homburg, Germany

Address all correspondence and requests for reprint to: Prof. Dr. Christoph Fusch, Department of Neonatology, University Children’s Hospital, Soldmannstrasse 15, D-17489 Greifswald, Germany. E-mail: fusch{at}mail.uni-greifswald.de

There is clear evidence that the placenta produces leptin. However, it is still unclear to what extent leptin is released into the maternal and the fetal circulation. The aim of our study was to determine placental leptin release rates into these 2 compartments. In 10 term placentas, using dual in vitro perfusion of an isolated cotyledon, concentrations of leptin, hCG, and human placental lactogen (hPL) were determined in perfusates and in the tissue before and after perfusion. With perfusions lasting 270–840 min, total 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 circulation (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 results. Release into the fetal circulation correlated significantly with release into the maternal circulation for leptin (r = 0.648; P < 0.05) and hPL (r = 0.721; P < 0.05). Furthermore, release of leptin into the fetal circulation 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 circulation, but compared with other placental hormones (hCG and hPL), a considerably higher proportion of leptin is released into the fetal circulation. These findings may at least partially explain the marked increase in maternal serum leptin levels in pregnancy. The rapid postnatal decrease in leptin levels in both the mother and the neonate is also consistent with the concept of placental origin.

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