Maternal diabetes has several adverse effects on embryogenesis and fetal development and causes multiple congenital anomalies, and secondary medical complications collectively referred to as diabetic embryopathy. Diabetic mothers have 2-3 times more chances of having a gestation affected with birth defects than non-diabetic mothers. High maternal blood glucose itself is a major teratogenic agent as it alters many normal signaling pathways involved in fetal development and organogenesis, though the exact cellular reason for teratogenicity is not clear.
Maternal high serum glucose level alters maternal as well as fetal metabolism. Both maternal and fetal hyperglycemia and ketosis have a role in pathogenesis. Environmental (maternal diabetes and intrauterine condition) and genetic predisposition interplay adversely in organogenesis. The congenital malformation is likely to have occurred in early gestation because organogenesis occurs in the first trimester, and increased maternal metabolic dysregulation increases the risk of giving birth with congenital malformations.
Even women with good diabetes control with insulin and tight glycemic index control show increased malformation and behavioral impairment as compared to the general population without diabetes. The diabetic status of the father does not play a role in causing malformations. However, paternal type 1 diabetes increases the risk of diabetes in children later in life. Children born from diabetic mothers may show lower mental and psychomotor scores later in life.
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