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BOR - Papers in Press, published online ahead of print July 21, 2004.
Biol Reprod 2004, 10.1095/biolreprod.104.031112
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BIOLOGY OF REPRODUCTION 71, 1746–1752 (2004)
DOI: 10.1095/biolreprod.104.031112
© 2004 by the Society for the Study of Reproduction, Inc.


Pregnancy

Two Isoforms of the Leptin Receptor Are Enhanced in Pregnancy-Specific Tissues and Soluble Leptin Receptor Is Enhanced in Maternal Serum with Advancing Gestation in the Baboon1

Deborah E. Edwards3,6, Rudolf P. Bohm, Jr7, Jeanette Purcell7, Marion S. Ratterree7, Kenneth F. Swan3, V. Daniel Castracane8, and Michael C. Henson2,3,4,5,6,7

Departments of Obstetrics and Gynecology,3 Structural and Cellular Biology,4 Physiology5; Interdisciplinary Program in Molecular and Cellular Biology6; and Tulane National Primate Research Center,7 Tulane University Health Sciences Center, New Orleans, Louisiana 70112 Department of Obstetrics and Gynecology8 and the Women's Health Research Center of Amarillo, Texas Tech University Health Sciences Center, Amarillo, Texas 79106

Leptin is a polypeptide hormone produced by adipose and other endocrine tissues. Although it has been linked to receptor-mediated pathways that directly influence human conceptus development, mechanisms that regulate the leptin receptor in pregnancy-specific tissues remain unclear. Therefore, we assessed leptin-receptor ontogeny and regulation in the baboon (Papio sp.), a primate model for human pregnancy. Placentae, decidua, and amniochorion were collected from baboons in early (Days 54–63, n = 4), mid (Days 98–103, n = 4), and late (Days 159–165, n = 4) gestation. Regulation by estrogen was assessed by elimination of androgen precursors via removal of the fetus (fetectomy) at midgestation and collection of tissues in late gestation (n = 4; term, ~184 days). Maternal serum was sampled with advancing gestation, and the abundance of soluble leptin receptor (solLepR), a potential mediator of gestational hyperleptinemia, was determined. Two placental leptin-receptor isoforms (130 and 150 kDa) increased (P < 0.04 and P < 0.02, respectively) in abundance with advancing gestation. Similarly, the 130-kDa isoform increased approximately fourfold (P < 0.0025) in decidua and approximately 10-fold (P < 0.015) in amniochorion between early and late gestation. Following fetectomy, maternal serum estradiol levels declined approximately 85% (P < 0.03), and the 150-kDa placental leptin-receptor isoform was reduced by more than half (P < 0.002). Maternal serum solLepR concentrations were correlated with gestational age (r = 0.52, P < 0.01) and were unaffected by fetectomy. The presence of leptin-receptor isoforms in pregnancy-specific tissues further denoted leptin's potential to directly influence conceptus development, whereas the 130-kDa solLepR identified in maternal serum suggested a means to facilitate the hyperleptinemia typical of primate pregnancy. Although estrogen did not appear to be the principal regulator of solLepR, it and other factors linked to advancing gestation may be implicated in the regulation of leptin-receptor synthesis.

1 Supported by NIH P51 RR00164 awarded to the Tulane National Primate Research Center.

2 Correspondence: Michael C. Henson, Department of Obstetrics and Gynecology, Tulane University Health Sciences Center, 1430 Tulane Avenue, New Orleans, LA 70112-2699. FAX: 504 988 1846; henson{at}tulane.edu




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