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Embryonic malformations in rats, resulting from maternal diabetes: preliminary observations
Journal of Embryology and Experimental Morphology
|October 1, 1977
Summary
Maternal diabetes, induced by alloxan or streptozotocin in rats, significantly increased fetal abnormalities like neural tube defects and heart deformities. Mild or pre-diabetic conditions also pose risks to fetal development.
Area of Science:
- Reproductive Biology
- Developmental Toxicology
- Endocrinology
Background:
- Maternal diabetes is a known risk factor for congenital anomalies.
- The specific mechanisms linking diabetes to teratogenesis require further elucidation.
Purpose of the Study:
- To investigate the teratogenic effects of chemically induced diabetes in pregnant rats.
- To identify specific fetal abnormalities associated with maternal diabetes.
Main Methods:
- Diabetes mellitus was induced in female Wistar rats using alloxan or streptozotocin.
- Embryonic and fetal development was assessed at mid-gestation and day 20.
- Fetal examinations included external morphology and X-ray analysis.
Main Results:
- Diabetic rats exhibited significantly higher incidences of fetal brain and heart abnormalities (7.5%) compared to controls (2.2%).
- Increased fetal resorptions (25% vs 7.2%) were observed in diabetic dams.
- Specific malformations included exomphalos, micrognathia, and incomplete sacral ossification.
Conclusions:
- Alloxan and streptozotocin-induced diabetes in rats leads to a spectrum of fetal malformations.
- Even mild or pre-diabetic states may increase fetal risk, potentially via fetal hyperinsulinism.
- These findings highlight the critical importance of glycemic control during pregnancy.
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