title: Significant increase in maternal plasma leptin concentration in induced delivery: a possible contribution of pro-inflammatory cytokines to placental leptin secretion.
abstract: Maternal plasma leptin concentration is significantly increased during pregnancy. However, its roles in pregnancy, especially in labor, have not been fully clarified. We measured plasma leptin concentrations in pregnant women during the course of induced labor, just after spontaneous vaginal delivery and Cesarean section at term. We also studied the regulation of leptin secretion from term placental tissue and BeWo cells, a trophoblastic cell-line. Plasma leptin concentrations increased significantly during labor (58.9 +/- 9.2 ng/ml) compared to those before labor induction (37.5 +/- 5.8 ng/ml, P<0.05), then decreased 3-6 days postpartum (14 +/- 3 ng/ml, n = 6, P<0.0001) to the levels of normal nonpregnant women. Leptin concentrations within an hour and 24 hours after spontaneous vaginal delivery were significantly higher than those after Cesarean section (P<0.05 for both comparisons). Similarly, leptin mRNA expression in placental tissues obtained after spontaneous vaginal delivery was significantly greater than that in those obtained after Cesarean section without labor (P<0.05). IL-1alpha and TNF-alpha treatment significantly stimulated leptin secretion and leptin mRNA expression in explant culture of human term placental tissue and in BeWo cells as compared with those in vehicle controls (P<0.05, for all comparisons). By contrast, oxytocin and prostaglandin F(2alpha) treatment had no effects on leptin secretion from explant culture of human term placental tissue or from BeWo cells. These data indicate that pro-inflammatory cytokines might stimulate placental leptin secretion, thus finally contributing to the increase in plasma leptin concentration during labor.
authors.affiliation: Department of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Japan.
authors.forename: Mercy A
authors.initials: MA
authors.lastname: Nuamah
authors.forename: Shigeo
authors.initials: S
authors.lastname: Yura
authors.forename: Norimasa
authors.initials: N
authors.lastname: Sagawa
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Itoh
authors.forename: Hiroko
authors.initials: H
authors.lastname: Mise
authors.forename: Daizo
authors.initials: D
authors.lastname: Korita
authors.forename: Kazuyo
authors.initials: K
authors.lastname: Kakui
authors.forename: Maki
authors.initials: M
authors.lastname: Takemura
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Ogawa
authors.forename: Kazuwa
authors.initials: K
authors.lastname: Nakao
authors.forename: Shingo
authors.initials: S
authors.lastname: Fujii
mesh_terms: D000328:Adult; D002460:Cell Line; D002585:Cesarean Section; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology*; D007751:Labor, Induced; D020738:Leptin / Q000097:blood* / Q000235:genetics / Q000378:metabolism; D009994:Osmolar Concentration; D010920:Placenta / Q000378:metabolism; D011247:Pregnancy / Q000097:blood*; D012333:RNA, Messenger / Q000378:metabolism; D046509:Tissue Culture Techniques; D014327:Trophoblasts / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
chemical_list: D007375:Interleukin-1; D020738:Leptin; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha