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Neural tube defects in diabetic embryopathy

Maternal diabetes increases the rate of congenital malformations in embryos, causing diabetic embryopathy which mostly affects hart and neural tube. In this work, we have employed inbred non-obese diabetic (NOD) mouse strain maintained at the Rudjer Boskovic Institute animal facility, in order to assess the incidence of neural tube defects (NTDs) in diabetic condition. NTDs are the consequence of the failed neural tube closure which can occur at different levels along rostrocaudal body axis, producing distinct morphological features with affected brain (exencephaly), spine (spina bifida aperta) or entire neural tube (craniorachischisis). We analyzed embryos from 15 non-diabetic and 15 alloxan-induced diabetic pregnancies at 10.5 days post coitum (time- point at which the neurulation in mice is completed). Both groups yielded nearly the same total number of implants. Embryos were categorized according to external morphology as normal, malformed, affected by NTD or resorbed. There was no significant difference between groups in crown-rump length and somite number of morphologically normal embryos. No significant difference between groups was observed in any category except NTDs, which occurred exclusively in diabetic pregnancies. Out of 15 analyzed diabetic pregnant females, 11 of them had embryos affected by at least one form of non-syndromic open NTD: overall 17 exencephalic embryos were found, 2 embryos had spina bifida aperta and 4 embryos had craniorachischisis. Obtained data suggest high specificity and sensitivity of the NOD model of diabetic embryopathy, which makes it particularly suitable and advantageous over other strains for studying the influence of maternal hyperglycemia on neurulation.

neural tube defects; diabetic embryopathy; non-obese diabetic mice

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