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a Department of Biology, Boston University, Boston, Massachusetts 02215
ABSTRACT
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.
First decision: 19 December 1999.
1 Supported by National Science Foundation (NSF) grants IBN9513926 (E.P.W.), IBN 9875871 (E.P.W. and T.H.K.), and DBI965157 (Research Experiences for Undergraduates) to T.H.K.; the Endocrine Society Student Summer Research Fellowship Program to B.A.S.; and fellowships from the Rothschild Foundation and the Fulbright Foundation to N.K.S. B.A.S, E.B., and P.T.M. were participants in Boston University's NSF-REU Site Program. R.U. and S.Z. were supported by an NSF-REU supplement to NSF grant IBN 9875871.
2 Correspondence: Eric P. Widmaier, Department of Biology, Boston University, 5 Cummington Street, Boston, MA 02215. FAX: 617 353 6340; widmaier{at}bio.bu.edu
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