Author(s): Schubring C, Kiess W, Englaro P, Rascher W, Dtsch J,
Abstract Share this page
Abstract The mechanisms by which maternal and fetal weight are regulated during pregnancy are poorly understood. The ob protein, termed leptin, is produced by adipocytes. It is involved in the regulation of body weight by suppressing appetite and stimulating energy expenditure both in humans and rodents. In this study we examined whether leptin concentrations in the mother and the newborn correlate with birth weight, placental weight, and maternal weight at term. Leptin concentrations were measured in amniotic fluid, venous and arterial cord blood, and maternal serum at birth (n = 27) using a specific RIA employing human recombinant leptin for tracer and standard preparation. Gestational age was 38-42 weeks, maternal age was 21-42 yr, mean maternal weight at birth was 80.0 +/- 10.8 kg, and mean body mass index before pregnancy was 23.4 +/- 2.8 kg/m2. The newborns' mean weight was 3450 +/- 580 g, and mean placental weight was 616 +/- 120 g. Serum leptin levels from nonpregnant women ranged between 1.7-18.4 ng/mL, median 5.5 ng/ml (n = 30). Mean leptin concentration in maternal serum at birth was 20.0 +/- 13.2 ng/mL and was higher (P < 0.002) than in arterial cord blood (9.7 +/- 9.4 ng/mL) and venous cord blood (8.9 +/- 8.6 ng/mL). Mean amniotic fluid leptin concentration was 3.6 +/- 2.8 ng/mL. Placental weight correlated inversely with leptin levels in maternal serum at birth (r = -0.49, P < 0.01). In addition, leptin concentrations in venous cord blood correlated significantly with the levels in arterial cord blood (r = 0.98, P < 0.0001), and leptin levels in cord blood correlated positively with birth weight (r = 0.57, P = 0.03) and placental weight (r = 0.50, P < 0.01). In contrast, there was no correlation between maternal serum leptin levels and birth weight. Thus, leptin levels are high in the fetus and in the mother at term. We hypothesize that high leptin levels could represent an important feed-back modulator of substrate supply and subsequently for adipose tissue status during late gestation.
This article was published in J Clin Endocrinol Metab
and referenced in Internal Medicine: Open Access