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Prenatal Leptin Production: Evidence That Fetal Adipose Tissue Produces Leptin

Service de Gynécologie-Obstétrique (J.L.), Hôpital Cochin–Saint Vincent-de-Paul, 75674 Paris; Université P. & M. Curie, Upres EA2396 (J.-C.C.), 75005 Paris; INSERM U 465 (M.G.-M., 75006 Paris; Centre National de la Recherche Scientifique UPR 1524 (M.C., S.H.-d.M.), 92120 Meudon; and INSERM U 449 (H.V.), 69372 Lyon, France

Address correspondence and requests for reprints to: Jacques Lepercq, M.D., Service de Gynécologie-Obstétrique, Hôpital Cochin–Saint Vincent-de-Paul, 82 avenue Denfert-Rochereau, 75674 Paris Cedex 14, France. E-mail: j.lepercq{at}svp.ap-hop-paris.fr

Abstract

In the adult, circulating leptin is highly correlated to adipose tissue mass. Whether such a relationship exists prenatally is unknown, because the actual source of fetal leptin has not been determined. In the present study, we have assessed the placental contribution to fetal and maternal circulating leptin concentrations and determined whether fetal adipose tissue produces leptin. The rate of leptin production in dually perfused human placenta was 0.036 ng/min·g. Ninety-five percent of the leptin released was delivered into the maternal circulation, vs. only 5% on the fetal side. Leptin messenger RNA and protein were detected in adipose tissue biopsies of 20–38 week human fetuses. However, leptin concentration was twice lower in fetal (0.22 ± 0.11 ng/mg protein, n = 6) than in adult (0.49 ± 0.12 ng/mg protein, n = 8) adipose tissue. Umbilical leptin levels closely reflected ponderal index at birth over a wide range of birth weights (1.6–4.1 kg). In sharp contrast, maternal and placental leptin concentrations were increased in pregnancies associated with fetal growth retardation.

We conclude that umbilical leptin levels are independent of placental leptin production and can be taken as a marker of fat mass in human fetuses. By contrast, placental leptin production makes a substantial contribution to maternal circulating leptin levels during pregnancy.

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