Correlation of metabolic characteristics with maternal, fetal and placental asprosin in human pregnancy

Endocr Connect. 2022 Mar 14;11(3):e220069. doi: 10.1530/EC-22-0069.

Abstract

Objective: Asprosin is a recently discovered hormone associated with obesity and diabetes mellitus. Little is known about asprosin's role during pregnancy, but a contribution of asprosin to pregnancy complications resulting from maternal obesity and gestational diabetes mellitus (GDM) is conceivable. We assessed the potential effects of obesity, GDM and other clinical parameters on maternal and fetal umbilical plasma asprosin concentrations and placental asprosin expression.

Design: The Cologne-Placenta Cohort Study comprises 247 female patients, from whom blood and placentas were collected at the University Hospital Cologne.

Methods: We studied the maternal and fetal umbilical plasma and placentas of pregnant women with an elective, primary section. Sandwich ELISA measurements of maternal and fetal umbilical plasma and immunohistochemical stainings of placental tissue were performed to determine the asprosin levels. Also, the relation between asprosin levels and clinical blood parameters was studied.

Results: There was a strong correlation between the maternal and fetal plasma asprosin levels and both increased with GDM in normal-weight and obese women. Asprosin immunoreactivity was measured in cultivated placental cells and placental tissue. BMI and GDM were not but pre-pregnancy exercise and smoking were correlated with maternal and/or fetal asprosin levels. Placental asprosin levels were associated with maternal but not with fetal plasma asprosin levels and with BMI but not with GDM. Placental asprosin was related to maternal insulin levels and increased upon insulin treatment in GDM patients.

Conclusions: Asprosin could potentially act as a biomarker and contribute to the clinical manifestation of pregnancy complications associated with maternal obesity.

Keywords: GDM; asprosin; exercise; insulin; obesity; placenta; smoking.