Growth retardation and dysmorphogenesis in the rat conceptus are accompanied by diminished tissue myo-inositol following culture from day 9.5 to 11.5 of development in the presence of increased amounts of glucose. Reductions of myo-inositol and increased malformations are not corrected by aldose reductase inhibitors. In contrast, supplementation of culture medium with myo-inositol (1.5 mg/ml) restores tissue myo-inositol content, lowers the incidence of dysmorphogenic embryos (from 51.1 to 28.6%, P<0.001) and reduces the incidence of neural tube defects to control levels (from 33.3 to 6%, P<0.001). These results suggest that myo-inositol depletion is involved in the mechanism of diabetic embryopathy.
|Number of pages||4|
|Journal||Israel Journal of Medical Sciences|
|State||Published - 1990|
- birth defects
- diabetes mellitus