Abstract

Objective: To examine maternal serum levels of leptin at 11-13 weeks gestation in normal and pathological pregnancies. Methods: Serum leptin, PAPP-A and uterine artery pulsatility index (PI) at 11-13 weeks were measured in 480 singleton pregnancies, including 240 with normal outcome, 60 that subsequently developed preeclampsia (PE), 60 that developed Gestational Diabetes Mellitus (GDM), 60 that delivered Large for Gestational Age (LGA) neonates and 60 that delivered small(SGA) neonates. Regression analysis was used to determine factors affecting maternal serum leptin concentration and from this model each value was expressed as Multiples of the Median (MoM). The median MoM values in the outcome groups were compared. Results: In the normal group serum leptin levels increased with maternal weight and decreased with maternal height. In the PE group, the median leptin (1.18 MoM, p=0.027) and uterine artery PI (1.25 MoM, p<0.0001) were increased and serum PAPP-A (0.72 MoM, p<0.0001) was decreased. There was no significant association between serum leptin and either uterine artery PI (p=0.983) or serum PAPP-A (p=0.403). In the SGA, LGA and GDM groups serum leptin MoM was not significantly different from the controls (p=0.621, p=0.385 and p=0.722, respectively). Conclusion: In conclusion, in pregnancies that develop PE, maternal serum leptin concentration at 11-13 weeks is increased in a manner not related to altered placental perfusion or function. In pregnancies complicated by the development of GDM or delivery of SGA or LGA neonates, serum leptin is not significantly altered.

Highlights

  • IntroductionIn pregnancy the maternal serum levels of leptin start rising in the first trimester prior to significant maternal weight gain, increase with gestation to reach a peak during the second or third trimester and decline shortly after delivery [4]

  • Leptin, an adipose tissue derived polypeptide hormone, is thought to play an important role in metabolism by reducing insulin secretion and through an action on hypothalamic receptors to decrease food intake and increase energy expenditure [1,2]. 75 leptin has anti-inflammatory and angiogenic properties and is involved in immune response and T cell activation [3].In pregnancy the maternal serum levels of leptin start rising in the first trimester prior to significant maternal weight gain, increase with gestation to reach a peak during the second or third trimester and decline shortly after delivery [4]

  • In the normal outcome group multiple regression analysis demonstrated that serum leptin increased with maternal weight and decreased with maternal height but there was no significant association with fetal Crown-Rump Length (CRL) (p=0.652), maternal age (p=0.196), racial origin (p=0.081), cigarette smoking (p=0.558), mode of conception (p=0.606) or parity (p=0.597)

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Summary

Introduction

In pregnancy the maternal serum levels of leptin start rising in the first trimester prior to significant maternal weight gain, increase with gestation to reach a peak during the second or third trimester and decline shortly after delivery [4]. The main determinant of circulating maternal leptin is visceral fat [5], an additional source is the placenta [6]. Studies at 7-10 weeks’ gestation reported that the concentration of leptin is four times higher in coelomic fluid than maternal serum reflecting the high production of the protein by trophoblast [7]. Previous studies have reported that levels of maternal serum or plasma leptin are altered in pathological pregnancies, including Gestational Diabetes Mellitus (GDM), Preeclampsia (PE) and pregnancies delivering Small for Gestational Age (SGA) neonates. Most studies have reported on pregnancies with established disease some have examined circulating levels in the first and second trimester before the clinical onset of the disease and reported contradictory results [8,9,10,11,12,13,14]

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