title: Possible role of placental leptin in pregnancy: a review.
abstract: Leptin was initially identified as an adipocyte-derived hormone that decreases food intake and body weight via its receptor in the hypothalamus. Subsequent animal studies revealed various physiologic functions of leptin. Leptin plays an essential role in reproduction by regulating gonadotropin-releasing hormone secretion from the hypothalamus. It also modulates glucose metabolism by increasing insulin sensitivity and activates the sympathetic nervous system. In humans, leptin is also produced by placental trophoblasts and is secreted into both the maternal and fetal circulation. Leptin production in the placenta is increased in pregnancies complicated with several pathologic conditions. Leptin gene expression in the placenta is augmented in severe preeclampsia, and maternal plasma leptin levels in severe preeclampsia are significantly higher than those in normotensive pregnant women. Leptin production in the placenta is also increased in diabetic pregnancy with insulin treatment. Furthermore, leptin is proposed to play a functional role in implantation by virtue of its stimulatory effect on matrix metalloproteinase expression in cytotrophoblast. Dysregulation of leptin metabolism and/or function in the placenta may be implicated in the pathogenesis of various disorders during pregnancy, such as recurrent miscarriage, gestational diabetes, intrauterine growth retardation, and preeclampsia. In this review, possible roles of placental leptin are discussed.
authors.affiliation: Department of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan. fetus@kuhp.kyoto-u.ac.jp
authors.forename: Norimasa
authors.initials: N
authors.lastname: Sagawa
authors.forename: Shigeo
authors.initials: S
authors.lastname: Yura
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Itoh
authors.forename: Kazuyo
authors.initials: K
authors.lastname: Kakui
authors.forename: Maki
authors.initials: M
authors.lastname: Takemura
authors.forename: Mercy A
authors.initials: MA
authors.lastname: Nuamah
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Ogawa
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Masuzaki
authors.forename: Kazuwa
authors.initials: K
authors.lastname: Nakao
authors.forename: Shingo
authors.initials: S
authors.lastname: Fujii
mesh_terms: D017667:Adipocytes / Q000378:metabolism; D004734:Energy Metabolism / Q000502:physiology; D005260:Female; D005333:Fetus / Q000502:physiology; D006801:Humans; D020738:Leptin / Q000097:blood / Q000378:metabolism / Q000502:physiology*; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy / Q000502:physiology*
chemical_list: D020738:Leptin