Placental expression of leptin: fetal sex-independent relation with human placental growth

Objectives Leptin (LEP) is a vital placental hormone that is known to affect different aspects of placental function and fetal development. The present study aimed to determine the association of placental LEP transcript abundance with maternal, placental, and newborn parameters. Subjects/methods In this retrospective case-control study, placental samples (n = 105) were collected from small (SGA) and appropriate (AGA) for gestational age full-term singleton pregnancies (n = 44 SGA and n = 61 AGA). Placental transcript abundance of LEP was assessed by real-time quantitative PCR after normalization to a reference gene panel. LEP methylation was measured using a quantitative MethyLight assay in a subset of samples (n = 54). Results Placental LEP transcript abundance was negatively and significantly associated with placental weight (beta = -3.883, P = 0.015). This association continued to be significant in the SGA group (beta = -10.332, P = 0.001), both in female (beta = -15.423, P = 0.021) and male births (beta = -10.029, P = 0.007). LEP transcript abundance was not associated with LEP methylation levels (Spearman's rho = 0.148, P = 0.287). Conclusion We conclude that placental upregulation of LEP is an integral and fetal sex-independent component of placental growth restriction, which can be potentially targeted through maternal dietary modifications to improve fetoplacental growth.