Abstract
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.
Original language | English |
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Pages (from-to) | 541-544 |
Number of pages | 4 |
Journal | Israel Journal of Medical Sciences |
Volume | 26 |
Issue number | 10 |
State | Published - 1990 |
Externally published | Yes |
Keywords
- Hyperglycemia
- birth defects
- diabetes mellitus
- inositol
- teratogenesis