Prenatal leptin production: Evidence that fetal adipose tissue produces leptin

In the adult, circulating leptin is highly correlated to adipose tissue mas s. Whether such a relationship exists prenatally is unknown, because the ac tual source of fetal leptin has not been determined. In the present study, we have assessed the placental contribution to fetal and maternal circulati ng leptin concentrations and determined whether fetal adipose tissue produc es 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 delivere d into the maternal circulation, vs, only 5% on the fetal side. Leptin mess enger RNA and protein were detected in adipose tissue biopsies of 20-38 wee k 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 protei n, n = 8) adipose tissue. Umbilical leptin levels closely reflected pondera l 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 pr egnancies associated with fetal growth retardation. We conclude that umbilical leptin levels are independent of placental lepti n production and can be taken as a marker of fat mass in human fetuses. By contrast, placental leptin production makes a substantial contribution to m aternal circulating leptin levels during pregnancy.