Decreased maternal serum adiponectin and increased insulin-like growth factor-1 levels along with increased placental glucose transporter-1 expression in gestational diabetes mellitus: Possible role in fetal overgrowth.

INTRODUCTION

The placental glucose transporter - 1 (GLUT-1) is involved in the transplacental glucose transport to the fetus. GLUT-1 expressions are increased in diabetic pregnancies and associated with altered fetal growth. However, the factors regulating the GLUT-1 expressions are largely unknown. We hypothesised that maternal adipokines and insulin-like growth factor-1 (IGF1) modulate the placental expressions of GLUT-1 through the activation of insulin/IGF-1 signalling which may contribute to a fetal overgrowth in GDM.

METHODS

Maternal blood, cord blood and placental samples were collected from GDM and control pregnant women (CPW). The biochemical parameters, IGF1, adipokines, and high sensitive C- reactive protein were measured. We analysed the placental expressions of GLUT-1 and proteins related to insulin/IGF-1 signalling - insulin receptor -β, insulin receptor substrate - 1, phosphatidylinositol-3-kinase p110α, phospho Akt-1, phospho extracellular signal-regulated kinase 1/2, and nuclear factor-κB p65 in GDM and CPW.

RESULTS

Increased maternal IGF-1 and decreased adiponectin levels were found in the GDM women. Maternal IGF-1 levels were positively correlated, whereas adiponectin levels were negatively correlated with the birth weight of GDM newborns. Increased phosphorylation of Akt and ERK 1/2 was found in the placenta of GDM women. Placental expressions of GLUT-1 were significantly higher in the GDM women and positively correlated to the maternal IGF-1 levels in the GDM group.

DISCUSSION

Decreased maternal adiponectin and increased IGF-1 levels might have caused increased GLUT-1 expression via the increased activation of insulin/IGF-1 signalling in the placenta of GDM women which might have influenced the fetal growth.