Placental leptin in normal, diabetic and fetal growth-retarded pregnancies

R.g. Lea, D Howe, L T Hannah, O Bonneau, L. Hunter, Nigel Hoggard

Research output: Contribution to journalArticle

139 Citations (Scopus)

Abstract

Leptin expression in third trimester placenta (p) and leptin concentrations in umbilical cord blood (cb) were investigated in normal pregnancies [n = 10 (p), 31 (cb)] and abnormal pregnancies complicated with (i) maternal insulin-dependent diabetes [IDDM: n = 3 (p), 13 (cb)], (ii) gestational diabetes [GD: n = 2 (p), 10 (cb)] and (iii) fetal growth retardation [FGR: n = 5 (p), 5 (cb)]. By in-situ hybridization and immunohistochemistry, placental leptin mRNA and protein were co-localized to the syncytiotrophoblast and villous vascular endothelial cells. Leptin receptor was immunolocalized to the syncytiotrophoblast. Relative to controls, the FGR group was characterized by low concentrations of placental and cord blood leptin. In a twin pregnancy, the normal-sized infant exhibited more placental and cord blood leptin than its growth-retarded twin. In contrast, both diabetic groups exhibited high concentrations of placental leptin mRNA and protein. The IDDM group exhibited the highest concentrations of leptin in cord blood. No change was observed in the expression of the leptin receptor in either the growth-retarded or diabetic pregnancies. In conclusion, the localization of placental leptin suggests that it may be released into both maternal and fetal blood. Furthermore, in fetal growth-retarded and diabetic pregnancies, the changes in leptin expression in the placenta and in leptin concentrations in umbilical cord blood appear to be related.
Original languageEnglish
Pages (from-to)763-769
Number of pages7
JournalMolecular Human Reproduction
Volume6
Issue number8
Publication statusPublished - 1 Aug 2000

Fingerprint

Fetal Development
Leptin
Fetal Blood
Pregnancy
Leptin Receptors
Trophoblasts
Type 1 Diabetes Mellitus
Placenta
Mothers
Pregnancy in Diabetics
Messenger RNA
Twin Pregnancy
Gestational Diabetes
Fetal Growth Retardation
Third Pregnancy Trimester
Growth
In Situ Hybridization
Proteins
Endothelial Cells
Immunohistochemistry

Keywords

  • Carrier Proteins
  • Diabetes Mellitus, Type 1
  • Female
  • Fetal Blood
  • Fetal Growth Retardation
  • Humans
  • Insulin
  • Leptin
  • Placenta
  • Pregnancy
  • Pregnancy Trimester, First
  • Pregnancy Trimester, Third
  • Pregnancy in Diabetics
  • Receptors, Cell Surface
  • Receptors, Leptin
  • Reference Values
  • diabetes
  • fetal
  • trophoblast

Cite this

Lea, R. G., Howe, D., Hannah, L. T., Bonneau, O., Hunter, L., & Hoggard, N. (2000). Placental leptin in normal, diabetic and fetal growth-retarded pregnancies. Molecular Human Reproduction, 6(8), 763-769.

Placental leptin in normal, diabetic and fetal growth-retarded pregnancies. / Lea, R.g.; Howe, D; Hannah, L T; Bonneau, O; Hunter, L.; Hoggard, Nigel.

In: Molecular Human Reproduction, Vol. 6, No. 8, 01.08.2000, p. 763-769.

Research output: Contribution to journalArticle

Lea, RG, Howe, D, Hannah, LT, Bonneau, O, Hunter, L & Hoggard, N 2000, 'Placental leptin in normal, diabetic and fetal growth-retarded pregnancies', Molecular Human Reproduction, vol. 6, no. 8, pp. 763-769.
Lea RG, Howe D, Hannah LT, Bonneau O, Hunter L, Hoggard N. Placental leptin in normal, diabetic and fetal growth-retarded pregnancies. Molecular Human Reproduction. 2000 Aug 1;6(8):763-769.
Lea, R.g. ; Howe, D ; Hannah, L T ; Bonneau, O ; Hunter, L. ; Hoggard, Nigel. / Placental leptin in normal, diabetic and fetal growth-retarded pregnancies. In: Molecular Human Reproduction. 2000 ; Vol. 6, No. 8. pp. 763-769.
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