Abstract
Introduction: Hyperglycemic conditions achieved during pregnancy have been shown to have detrimental effects to fetal development and increase the prevalence of childhood comorbidities. However, the mechanisms in which diabetic pregnancies affect placental development and subsequently contribute to adverse health effects on the mother and offspring remain unclear. Research design and methods: Streptozotocin was used to induce gestational diabetes in mice. In this model, hyperglycemia was established at embryonic day 3.5 (E3.5). Pregnancy mass was collected at E10.5, E12.5, E14.5, and E16.5 for different assessments. Results: Both placental and embryonic weights were found to be significantly elevated at E16.5. At E14.5, a significantly larger junctional zone with increased number of glycogen trophoblasts was found in the placentas from hyperglycemic pregnancies (HG group) compared to the placentas from normoglycemic pregnancies (NG group). Importantly, the HG placenta exhibited decreased trophoblast giant cell (TGC) association and TUNEL+ cells, and increased expression of α-SMA on the spiral artery, suggesting arterial remodeling was impacted. Moreover, the interhemal membrane of the labyrinth layer, was found to be thicker in the HG placentas. Furthermore, hyperglycemia resulted in more offspring congenital defects, which were associated with a thicker interhemal membrane. Conclusions: Together, these results suggest that gestational diabetes perturbs proper placental development and function, specifically spiral artery remodeling and angiogenesis, thereby negatively impacting embryonic development.
Highlights
Diabetes during pregnancy is known to affect the health of both mothers and their infants
The results showed a marginal significance of interhemal membrane (IHM) thickness and the congenital defects (p = 0.085), but not for the glycogen trophoblast (GlyT)/spongiotrophoblast cells (SpTs) ratio (p = 0.200), the lumen diameter (LD)/outer diameter (OD) ratio (p = 0.207) and the trophoblast giant cell (TGC)-spiral artery (SpA) association (p = 0.222) (Fig. 5J–L)
For the first time, this study demonstrated an association between IHM thickness and birth defects, the same was not observed with GlyT/junctional zone (JZ) nor LD/OD
Summary
Diabetes during pregnancy is known to affect the health of both mothers and their infants. Among the two types of diabetes during pregnancy, gestational diabetes (GDM) accounts for 90% and pre-gestational diabetes (PGDM) comprises the remaining 10% [1, 2]. With the introduction of insulin, diabeticassociated fetal mortality rates are reduced from 70% to nearly 12%. The present birth defect rate in diabetic pregnancies (~10%) is still higher than that of the general population (3%), and appears to be ever increasing [2,3,4,5,6]. It has been suggested that placental damages from diabetic pregnancies could be the cause of fetal complications observed in the human population [7]
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