Hyperleptinemia in pregnant bats is characterized by increased placental leptin secretion in vitro.

Hyperleptinemia is a common feature of pregnancy in mammals. The source of increased plasma leptin is uncertain. We examined leptin secretory rates in vitro to test the hypothesis that leptin secretion is upregulated during pregnancy. Two species of insectivorous bats were examined, Myotis lucifugus and Eptesicus fuscus, because of their unique reproductive cycle. Body mass and plasma leptin significantly increased with gestation and decreased during lactation. Adiposity increased in midgestation, then decreased in late gestation and lactation and was not significantly correlated with plasma leptin in pregnant or early lactating individuals. Leptin secretion in vitro per gram of adipose tissue tended to increase with gestation but was not significantly correlated with plasma leptin in the same individuals. Leptin secretion from placentae, however, increased with gestation and was significantly correlated with plasma leptin from the same individuals. In suckling pups, plasma leptin was high shortly after birth, then decreased to low levels that were not correlated with adiposity thereafter. We conclude that in bats, the placenta is a major source of circulating leptin during pregnancy, and that adiposity and plasma leptin levels are decoupled during three different periods of intense metabolic demand (pregnancy, early lactation, and neonatal growth).

Steroid-dependent up-regulation of adipose leptin secretion in vitro during pregnancy in mice.

Circulating leptin levels are elevated during the later stages of pregnancy in mammals, suggesting that maternal leptin may play a role in maintenance of pregnancy and/or preparation for parturition and lactation. The regulation and source of circulating leptin during pregnancy remains undetermined, but leptin mRNA levels increase in adipose tissue during this time in some species. Considerable controversy exists whether placenta is also a leptin-secreting tissue during pregnancy. Here, we directly demonstrate that leptin secretion rates from mouse adipose tissue in vitro are decreased during early pregnancy and up-regulated during late pregnancy and lactation. Changes in leptin secretion rates in vitro paralleled those of circulating leptin in vivo during gestation. Subcutaneous implants of estradiol or corticosterone into lactating mice for 48 h stimulated adipose leptin secretion rates in vitro to the level of that in pregnant mice. However, corticosterone, but not estradiol, increased leptin secretion when added to isolated adipose tissue in vitro. Placentae obtained at two stages of pregnancy did not secrete leptin in vitro, either when acutely isolated or when dissociated into cells for long-term cultures. Placental tissue (or cells) secreted progesterone, however, demonstrating placental viability. We conclude that hyperleptinemia during late pregnancy in mice primarily results from corticosterone-dependent up-regulation of leptin secretion from adipose tissue, and that the placenta does not contribute to leptin secretion. The initial decrease in leptin secretory rates from adipose tissue during early pregnancy may facilitate energy storage for the subsequent, increased metabolic demands of later pregnancy and lactation.