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Diabetes mellitus (DM) is a health condition characterized by hyperglycemia over a prolonged period. There are three main types of DM: DM type 1 (DM1), DM2 and gestational DM (GDM). Maternal diabetes, which includes the occurrence of DM1 and DM2 during pregnancy or GDM, increases the occurrence of gesttional complications and adverse fetal outcomes. The hyperglycemic intrauterine environment affects not only the fetus but also the placental development and function in humans and experimental rodents. The underlying mechanisms are still unclear, but some evidence indicates alterations in trophoblast proliferation, apoptosis and cell cycle control in diabetes. A proper coordination of trophoblast proliferation, differentiation and invasion is required for placental development. Initially, increased expression of proliferative markers in junctional and labyrinth zones of rat placentas and villous cytotrophoblast, syncytiotrophoblast, stromal cells and fetal endothelial cells in human placentas is reported among diabetics. Moreover, reduced apoptotic index and expression of some apoptotic genes are described in placentas of GDM women. In addition, cell cycle regulators including cyclins and cyclin-dependent kinase inhibitors seem to be affected by the hyperglycemic environment. More studies are necessary to check the balance between proliferation, apoptosis and differentiation in trophoblast cells during maternal diabetes.

The function of the visceral yolk sac (VYS) is critical for embryo organogenesis until final fetal development in rats, and can be affected by conditions such as diabetes. In view of the importance of diabetes during pregnancy for maternal and neonatal health, the objective of this study was to assess fetal weight, VYS cell markers, and viability in female Wistar rats (200-250 g) with induced diabetes (alloxan, 37 mg/kg) on the 8th gestational day (gd 8). At gd 15, rats from control (n=5) and diabetic (n=5) groups were anesthetized and laparotomized to remove the uterine horns for weighing of fetuses and collecting the VYS. Flow cytometry was used for characterizing VYS cells, and for determining mitochondrial activity, cell proliferation, DNA ploidy, cell cycle phases, and caspase-3 activity. Fetal weight was reduced in the diabetic group. Expression of the cell markers CD34, VEGFR1, CD115, CD117, CD14, CCR2, CD90, CD44, STRO-1, OCT3/4, and Nanog was detected in VYS cells in both groups. In the diabetic group, significantly decreased expression of CD34 (P<0.05), CCR2 (P<0.001), and OCT3/4 (P<0.01), and significantly increased expression of CD90 (P<0.05), CD117 (P<0.01), and CD14 (P<0.05) were observed. VYS cells with inactive mitochondria, activated caspase-3, and low proliferation were present in the rats with diabetes. Severe hyperglycemia caused by maternal diabetes had negative effects on pregnancy, VYS cell viability, and the expression of cell markers.

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Introduction:The objective of this study was to analyze the morphological structure of the heart and aorta of rats treated with the synthetic glucocorticoid dexamethasone. Material and Methods: Male Wistar rats were divided into two groups: 08 control rats undergoing treatment with a 0.9% saline solution for 10 days and 08 rats treated for 10 days with dexamethasone (2mg/kg animal weight). Results: Histological analysis detected a mild cardiac hypertrophy and 15% reduction of collagen located in the aorta of animals treated with glucocorticoid when compared to the control group. Conclusion: We conclude that treatment with dexamethasone for a period of 10 consecutive days is able to promote morphological changes in the structure of the heart chamber and, impair morphological structure of aorta.

Rodents have a well-developed visceral yolk sac (VYS) that acts as an active region for metabolic exchange and nutrition uptake until final fetal development in rats and may be affected by diabetes. Using Wistar rats, diabetes was induced by a single injection of alloxan at gestational day 8 (8 gd) and at 15 gd the collection of VYS was made. Flow cytometry was performed for VYS cell characterization, determination of mitochondrial activity, cell proliferation, DNA ploidy, cell cycle phases and caspase-3 activity. Fetal weight was reduced in the diabetic group. CD34, CCR2, and OCT3/4 expressions were significantly reduced, and CD90, CD117, and CD14 expressions were increased in the diabetic group. VYS cells with inactive mitochondria, activated caspase-3, and low proliferation were present in the diabetic condition. Severe hyperglycemia due to maternal diabetes was shown to have negative effects on pregnancy, VYS viability, and cell marker expression.