Abstract
The aim of this study was to assess placental changes and reproductive outcomes in neonatally induced mild diabetic dams and fetal development in their offspring. At birth, female rats were assigned either to control or diabetic group (100 mg of streptozotocin/Kg, subcutaneously). At adulthood, the female rats were mated. During pregnancy, the blood glucose levels and glucose and insulin tolerance tests were performed. At term, maternal reproductive outcomes, fetal and placental weight, and placental morphology were analyzed. Diabetic rats had smaller number of living fetuses, implantations and corpora lutea, and increased rate of embryonic loss. Placenta showed morphometric alterations in decidua area. Our results showed that mild diabetes was sufficient to trigger alterations in maternal organism leading to impaired decidua development contributing to failure in embryonic implantation and early embryonic losses. Regardless placental decidua alteration, the labyrinth, which is responsible for the maternal-fetal exchanges, showed no morphometric changes contributing to an appropriate fetal development, which was able to maintain normal fetal weight at term in mild diabetic rats. Thus, this experimental model of diabetes induction at the day of birth was more effective to reproduce the reproductive alterations of diabetic women.
Highlights
Pregnant women with type 1 or type 2 diabetes are at increased risk of miscarriage, stillbirth, congenital malformations, placental abnormalities, and intrauterine malprogramming
The Oral Glucose Tolerance Test (OGTT) showed an increase in blood glucose levels for diabetic rats at 0, 30, 60, and 120 min compared to control rats
Regarding the Insulin Tolerance Test (ITT) test, blood glucose levels were significantly higher in mild diabetic rats (MD) group at two timepoints (0 and 30 min) compared to the control group
Summary
Pregnant women with type 1 or type 2 diabetes are at increased risk of miscarriage, stillbirth, congenital malformations, placental abnormalities, and intrauterine malprogramming. Maternal diabetes is an unfavorable environment for embryonic and fetoplacental development [1,2,3,4,5,6,7] These important aspects of human diabetic pregnancies can be studied using the appropriate animal models [8], by ethical reasons and by the multiplicity of uncontrolled variables that may modify the intrauterine environment [9]. In a previous study conducted at our laboratory [19], experimental mild diabetes induced at 5 days of life was not effective in reproducing the reproductive outcomes (miscarriage, fetal viability, and morbidity) observed in diabetic pregnant women. In the cases that rats reached at term pregnancy, no repercussions were observed probably due to a maternal adaptive response to mild glycemic levels or placental changes. We hypothesized that another model of mild hyperglycemia
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