Placental nutrient transporter abundance in gestational diabetes mellitus with normal birthweight.

INTRODUCTION

Gestational diabetes mellitus (GDM) is associated with adverse pregnancy outcomes. When the infant is large for gestational age, placental nutrient transport capacity is often increased. We hypothesized that GDM alters placental nutrient transporter abundance irrespective of infant size.

METHODS

We determined the abundance of transporters in placentas from GDM women delivering normal birthweight infants (n = 8) and from normal glucose tolerance (n = 9) women, using an unbiased, global proteomics approach. Liquid chromatography mass-spectrometry was performed to determine relative quantity of placental proteins in villous tissue. Differentially expressed proteins were computed and gene ontology analysis used to identify glucose, amino acid, and fatty acid transporters. Selected nutrient transporter genes were also measured using qRT-PCR and cell signalling molecule abundances assessed by Western blot.

RESULTS

Neonatal birthweight was similar in GDM and normal glucose tolerance groups (P > 0.05). In the GDM placenta, the abundances of monocarboxylate transporter 10 (MCT10), fatty acid-binding protein 3 (FABP3), and retinol binding-protein 1 (RBP1) were reduced compared to the normal glucose tolerance controls (P < 0.05, log fold change < -0.5). The other 18 nutrient transport proteins identified did not differ in abundance between GDM and control placentas. Gene expressions of glucose transporter SLC2A9, amino acid transporters SLC38A2 and SLC38A4, and fatty acid transporter SLC27A6 were downregulated in GDM placentas (P < 0.05).

CONCLUSION

GDM does not increase placental nutrient transporter abundance when birthweight is within the normal range. Downregulation of some transporters, together with vascular perfusion, more likely affect pregnancy outcome and metabolic development of the infant.