title: Placental leptin in normal, diabetic and fetal growth-retarded pregnancies.
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.
authors.affiliation: Division of Nutrition and Development, Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK.
authors.forename: R G
authors.initials: RG
authors.lastname: Lea
authors.forename: D
authors.initials: D
authors.lastname: Howe
authors.forename: L T
authors.initials: LT
authors.lastname: Hannah
authors.forename: O
authors.initials: O
authors.lastname: Bonneau
authors.forename: L
authors.initials: L
authors.lastname: Hunter
authors.forename: N
authors.initials: N
authors.lastname: Hoggard
mesh_terms: D002352:Carrier Proteins / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000378:metabolism*; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D005317:Fetal Growth Retardation / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000235:genetics / Q000378:metabolism*; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D011261:Pregnancy Trimester, First; D011263:Pregnancy Trimester, Third; D011254:Pregnancy in Diabetics / Q000378:metabolism*; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D012016:Reference Values
chemical_list: D002352:Carrier Proteins; D007328:Insulin; C515448:LEPR protein, human; D020738:Leptin; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin