Abstract

Altered fetal growth, either reduced or exacerbated, is associated with adverse perinatal outcomes. The underlying pathogenetic mechanisms of altered growth remain unclear. Fibroblast growth factor 21 (FGF21) and insulin are both considered to be major regulators of tissue growth and metabolism. The aim of our study was to investigate the association of second trimester amniotic fluid FGF21 and insulin concentrations with fetal growth. The amniotic fluid concentrations of FGF21 and insulin were determined in 80 cases of different fetal growth patterns (SGA—small for gestational age, LGA—large for gestational age, and AGA—appropriate for gestational age fetuses). Both peptides were found to be increased in cases of abnormal fetal growth, reduced growth velocity (SGA), or macrosomia (LGA). Specifically, FGF21 was significantly increased, as higher FGF21 levels were observed in the amniotic fluid of SGA and LGA fetuses compared with AGA fetuses (p < 0.05). Furthermore, the more severe the fetal smallness, the higher the FGF21 levels (p < 0.05). Similarly, higher insulin levels were noted in the amniotic fluid of SGA and LGA fetuses compared with those in AGA fetuses, though this was not statistically significant (p > 0.05). Again, the more severe the reduced fetal growth, the higher the insulin levels.

Highlights

  • IntroductionFetal growth velocity abnormalities (small for gestational age, SGA; large for gestational age, LGA) are associated with adverse perinatal outcomes compared with appropriate for gestational age (AGA) fetuses [1,2,3]

  • Fetal growth velocity abnormalities are associated with adverse perinatal outcomes compared with appropriate for gestational age (AGA) fetuses [1,2,3]

  • The study sample was 31 small for gestational age (SGA) fetuses, 18 LGA fetuses, and 31 AGA fetuses, all matched for gestational age, fetal sex, maternal weight, and height

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Summary

Introduction

Fetal growth velocity abnormalities (small for gestational age, SGA; large for gestational age, LGA) are associated with adverse perinatal outcomes compared with appropriate for gestational age (AGA) fetuses [1,2,3]. In the context of normal pregnancy, uterine spiral arteries undergo transformation from high-resistance and low-capacity vessels to low-resistance and high-capacity vessels, thereby enhancing placental perfusion and ensuring adequate blood supply to the fetus and, subsequently, normal fetal development [14]. When, this extravillous trophoblast remodeling process is defective, placental perfusion is limited, leading to placental ischemia and fetal growth restriction [15]

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