Background: Studies have identified that diseases in pregnancy affect fetal growth and development of the newborn. In Mexican population, the gene SLC16A11 has been identified as a factor that increases the risk of developing type 2 diabetes mellitus. To date, information is scarce about its expression in gestational diabetes mellitus (GDM); epigenetic modifications due to maternal hyperglycemic state could be identified early in fetal development.
Purpose: This study aimed to determine the SLC16A11 expression and methylation status in umbilical cord blood of newborns offspring of mothers with or without GDM.
Methods: Cross-sectional, analytic study. Pregnant patients undergoing caesarean delivery with and without GDM in the Unidad Medica de Alta Especialidad Hospital de Gineco-obstetricia #4 Luis Castelazo Ayala, Instituto Mexicano del Seguro Social, were invited to participate. DNA was extracted from the mothers' blood cells, or umbilical cord blood cells of their newborns, and subjected to methylation status. Total RNA was used to evaluate the SLC16A11 expression by endpoint RT-PCR. Variables were analyzed with Student t. Values of p <0.05 were considered statistically significant.
Results: A SLC16A11 downregulation was observed for newborns, while methylation status was found in only 1 of 68 mother-child pairs. Somatometry of newborns showed no differences between groups. Differences were found in total cholesterol, triglycerides, ALT, glucose, and HbA1c.
Conclusions: For the first time, a differential expression for SLC16A11 was observed in offspring. Downregulation in this gene expression could characterize the offspring from GDM. No difference was found in somatometry of newborns of mothers with and without GDM.
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