Abstract
Diabetes mellitus during pregnancy is a risk factor for improper closure of the neural tube during embryonic development. It is likely that this occurs via several parallel pathways. Previously proposed pathways for diabetic teratogenesis during neural tube closure include augmented production of nitric acid; reduction of Pax3; and increased production of long-chain acyl-CoA synthetase 1 (ACSL1). In the current discussion, an additional hypothesis is offered: that hyperglycemia might exert its teratogenic effects on the developing embryo via overexpression of collagen IV, leading to collagen imbalance and errors of remodelling.
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