Abstract

Objectives. Gestational diabetes mellitus (GDM) leads to an abnormal placental environment which may cause some structural alterations of placenta and affect placental development and function. In this study, the ultrastructural appearances of term placentas from women with GDM and normal pregnancy were meticulously compared. Materials and Methods. The placenta tissues of term birth from 10 women with GDM and 10 women with normal pregnancy were applied with the signed informed consent. The morphology of fetomaternal interface of placenta was examined using light microscopy (LM) and transmission electron microscopy (TEM). Results. On LM, the following morphological changes in villous tissues were found in the GDM placentas when compared with the control placentas: edematous stroma, apparent increase in the number of syncytial knots, and perivillous fibrin deposition. On TEM, the distinct ultrastructural alterations indicating the degeneration of terminal villi were found in the GDM placentas as follows: thickening of the basal membrane (BM) of vasculosyncytial membrane (VSM) and the VSM itself, significantly fewer or even absent syncytiotrophoblastic microvilli, swollen or completely destroyed mitochondria and endoplasmic reticulum, and syncytiotrophoblasts with multiple vacuoles. Conclusion. Ultrastructural differences exist between GDM and control placentas. The differences of placenta ultrastructure are likely responsible for the impairment of placental barrier and function in GDM.

Highlights

  • Gestational diabetes mellitus (GDM) is defined as the glucose intolerance with onset or first recognition during pregnancy [1]

  • The present study is the first to investigate systematically the ultrastructural changes in human term placentas derived from women with GDM

  • Mayhew et al found that those changes in the preeclampsia placenta were related to the fetal intrauterine growth restriction (IUGR), including the exchange surface areas, diffusion distances, and villous membrane diffusive conductance [17]

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Summary

Introduction

Gestational diabetes mellitus (GDM) is defined as the glucose intolerance with onset or first recognition during pregnancy [1]. The short-term adverse outcomes include macrosomia, neonatal hypoglycemia, neonatal jaundice, preeclampsia, preterm delivery, and cesarean delivery, while the longterm complications include obesity, abnormal glucose tolerance and diabetes in adolescence, or early adulthood. Placenta plays critical roles during pregnancy, including the exchange of nutrients, water, respiratory gases, and waste products and the synthesis of various hormones which regulate the transport of maternal fuels to the fetus and facilitate maternal metabolic adaptation to different pregnancy stages. These functions are determined by the structure, ultrastructure, and function of the placental exchange barrier. The increased thickness of VSM and reduced area of exchange related to fetal hypoxia appear to subject fetus to considerable risks [8]

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