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

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 ins ulin-dependent diabetes [IDDM: n = 3 (p), 13 (cb)], (ii) gestational diabet es [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 vi llous vascular endothelial cells. Leptin receptor was immunolocalized to th e syncytiotrophoblast, Relative to controls, the FGR group was characterize d by low concentrations of placental and cord blood leptin. In a twin pregn ancy, the normal-sized infant exhibited more placental and cord blood lepti n than its growth-retarded twin. In contrast, both diabetic groups exhibite d 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-ret arded 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 chang es in leptin expression in the placenta and in leptin concentrations in umb ilical cord blood appear to be related.