title: Role of leptin in pregnancy--a review.
abstract: Leptin is an adipocyte-derived hormone that decreases food intake and body weight via its receptor in the hypothalamus. In rodents, it also modulates glucose metabolism by increasing insulin sensitivity. We previously reported that leptin is produced by human placental trophoblasts. We also revealed that leptin gene expression in the placenta was augmented in severe pre-eclampsia, and suggested that placental hypoxia may play a role in this augmentation. Maternal plasma leptin levels correlated well with mean blood pressure, but not with body mass index. Plasma leptin levels in pre-eclamptic women with IUGR were higher than those without IUGR (P< 0.05). We further examined the effects of hyperleptinemia on the course of pregnancy by using transgenic mice (Tg) overexpressing leptin. In pregnant Tg mice, food intake was significantly less than non-Tg, and the fetal body weights were reduced to approximately 70 per cent of those of non-Tg. Resistin is a novel adipocyte-derived hormone that decreases insulin sensitivity and increases plasma glucose concentration, thus contributing the development of obesity-related type II diabetes mellitus. We recently found that resistin gene is expressed in the human placenta as well as adipose tissue. In this review, possible roles of placental leptin and resistin are discussed.
authors.affiliation: Department of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. fetus@kuhp.kyoto-u.ac.jp
authors.forename: N
authors.initials: N
authors.lastname: Sagawa
authors.forename: S
authors.initials: S
authors.lastname: Yura
authors.forename: H
authors.initials: H
authors.lastname: Itoh
authors.forename: H
authors.initials: H
authors.lastname: Mise
authors.forename: K
authors.initials: K
authors.lastname: Kakui
authors.forename: D
authors.initials: D
authors.lastname: Korita
authors.forename: M
authors.initials: M
authors.lastname: Takemura
authors.forename: M A
authors.initials: MA
authors.lastname: Nuamah
authors.forename: Y
authors.initials: Y
authors.lastname: Ogawa
authors.forename: H
authors.initials: H
authors.lastname: Masuzaki
authors.forename: K
authors.initials: K
authors.lastname: Nakao
authors.forename: S
authors.initials: S
authors.lastname: Fujii
mesh_terms: D000328:Adult; D000818:Animals; D004435:Eating / Q000502:physiology; D005260:Female; D020567:Fetal Weight / Q000502:physiology; D006729:Hormones, Ectopic / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins; D020738:Leptin / Q000235:genetics / Q000378:metabolism*; D008431:Maternal-Fetal Exchange; D051379:Mice; D008822:Mice, Transgenic; D020932:Nerve Growth Factor; D010920:Placenta / Q000378:metabolism* / Q000503:physiopathology; D010927:Placental Insufficiency / Q000378:metabolism / Q000503:physiopathology; D011225:Pre-Eclampsia / Q000097:blood; D011247:Pregnancy / Q000378:metabolism*; D011270:Pregnancy, Animal / Q000097:blood / Q000502:physiology*; D011506:Proteins; D052243:Resistin
chemical_list: D006729:Hormones, Ectopic; D036341:Intercellular Signaling Peptides and Proteins; D020738:Leptin; D011506:Proteins; C499624:RETN protein, human; C486574:RETNLB protein, human; D052243:Resistin; C499623:Retn protein, mouse; C413576:Retnla protein, mouse; D020932:Nerve Growth Factor