Keywords
Hydroxysteroid dehydrogenases
Immunohistochemistry
Maternal obesity
Placenta
Chorionic Villi
Glucocorticoids
How to Cite
Abstract
Context: An obesogenic maternal environment can directly impact both placental function and fetal growth and development. The enzyme 11? Hydroxysteroid Dehydrogenase type 2 (11?-HSD2), located in syncytiotrophoblast, inactivates cortisol converting it into cortisone to limit its direct passage to fetal circulation. Several studies propose that high glucocorticoid exposure is associated with reduced head circumference at birth, increased distractibility and inattention, among other alterations.
Objective: To determine the protein expression of 11?-HSD2 in term placenta samples classified according to BMI.
Methodology: Analytical cross-sectional study. For the development of the research, a population of 300 pregnant women who attended labor at an IPS in the city of Cali was recruited and a sample of 15 placental tissues (5 from each group classified according to BMI) was chosen to fulfill the objective of this study after signing an informed consent form. Placental tissue samples from pregnant women classified according to BMI were analyzed by immunohistochemistry for the 11?-HSD2 enzyme. Immunolabeling was evaluated by Image Pro Plus V 6.0 software. Results are shown as mean ± SE. Significant differences were considered when p < 0.05
Results: The 11?-HSD2 enzyme was expressed in the cytoplasm of the syncytiotrophoblast lining the ccgplacental villi; its expression was lower in placentas from women with pregestational obesity compared to placentas from normopese women (p< 0.05). Therefore, statistically significant differences were found between the two groups.
Conclusion: Starting gestation in a state of obesity affects the protein expression of the enzyme 11?-HSD2, which would compromise the control of cortisol levels reaching the fetal circulation.
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