Augmented placental production of leptin in preeclampsia: Possible involvement of placental hypoxia

Hiroko Mise, Norimasa Sagawa, Tsunekazu Matsumoto, Shigeo Yura, Hidetaka Nanno, Hiroaki Itoh, Takahide Mori, Hiroaki Masuzaki, Kiminori Hosoda, Yoshihiro Ogawa, Kazuwa Nakao

Research output: Contribution to journalArticlepeer-review

265 Citations (Scopus)

Abstract

Preeclampsia (PE) is a hypertensive disorder, which develops in late pregnancy and is usually associated with placental hypoxia and dysfunction. We have recently demonstrated that leptin is a novel placenta-derived hormone in humans and suggested its significance in human pregnancy (see Ref. 19). To explore the changes in the leptin production in placenta in PE, we measured the plasma leptin level and placental leptin messenger RNA expression in pregnant women with PE. Plasma leptin levels in preeclamptic women were elevated significantly, compared with gestational age- and body mass index- matched normal pregnant women (P < 0.0001). Plasma leptin levels in the severe PE group were significantly higher than those in the mild PE group (P < 0.0001). Plasma leptin levels in preeclamptic women were reduced, soon after the placental delivery, to those expected for their body mass indices. Northern blot analysis revealed that leptin messenger RNA levels are increased in the placentas from preeclamptic women, compared with normal pregnant women. Leptin secretion was increased significantly in a human trophoblastic cell line (BeWo cells) cultured under hypoxic conditions (5% O2), compared with those cultured under standard conditions (20% O2; P < 0.01). The present study demonstrated that placental production of leptin is augmented in severe PE, probably because of placental hypoxia, thereby suggesting the possible significance of leptin as a marker of placental hypoxia in severe PE.

Original languageEnglish
Pages (from-to)3225-3229
Number of pages5
JournalJournal of Clinical Endocrinology and Metabolism
Volume83
Issue number9
DOIs
Publication statusPublished - 1998
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

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