Genetic and environmental influence on diabetic rat embryopathy.

@article{Ejdesj2011GeneticAE,
  title={Genetic and environmental influence on diabetic rat embryopathy.},
  author={Andreas Ejdesj{\"o} and Parri Wentzel and Ulf J. Eriksson},
  journal={American journal of physiology. Endocrinology and metabolism},
  year={2011},
  volume={300 3},
  pages={
          E454-67
        }
}
We assessed genetic and environmental influence on fetal outcome in diabetic rat pregnancy. Crossing normal (N) and manifestly diabetic (MD) Wistar Furth (W) and Sprague-Dawley (L) females with W or L males yielded four different fetal genotypes (WW, LL, WL, and LW) in N or MD rat pregnancies for studies. We also evaluated fetal outcome in litters with enhanced or diminished severity of maternal MD state, denoted MD(+)WL and MD(-)LW. The MDWW litters had less malformations and resorptions (0… 
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Influence of maternal metabolism and parental genetics on fetal maldevelopment in diabetic rat pregnancy.
TLDR
Together with fetal differences in enzymatic activity and expression of Gapdh, ROS scavengers, and developmental genes, these results may suggest a teratological mechanism in diabetic pregnancy influenced by maternal metabolism and parental strain epigenetics.
Linkage study of embryopathy-polygenic inheritance of diabetes-induced skeletal malformations in the rat.
Distinct effects of short- and long-term type 1 diabetes to the placental extracellular matrix and fetal development in mice.
Hyperglycemia induces embryopathy, even in the absence of systemic maternal diabetes: an in vivo test of the fuel mediated teratogenesis hypothesis.
Perturbation of Retinoid Homeostasis Increases Malformation Risk in Embryos Exposed to Pregestational Diabetes
TLDR
It is found that Cyp26a1, which encodes a key enzyme for catabolic inactivation of RA required for tight control of local RA concentrations, is significantly downregulated in embryos of diabetic mice, providing new insight into gene–environment interactions that influence individual risk in the manifestation of diabetes-related birth defects.
Receptor for advanced glycation end products (RAGE) knockout reduces fetal dysmorphogenesis in murine diabetic pregnancy.
DIABETES MELLITUS EXPERIMENTAL: ESTUDIO MORFOMÉTRICO EN LA DESCENDENCIA DE RATAS DIABÉTICAS EXPERIMENTAL DIABETES MELLITUS: MORPHOMETRIC STUDY IN THE PROGENY OF DIABETIC RATS
TLDR
In fetuses of diabetic rats independent of treatment there was a decrease in the values of size and weight, and with respect to the control fetuses an increase of the anteroposterior and biparietal diameters and differences in facial morphometry variables.
The status of diabetic embryopathy
TLDR
The experimental work in this field has revealed a partial, however complex, answer to the teratological question, and some of the latest suggestions are reviewed.
Modeling anterior development in mice: Diet as modulator of risk for neural tube defects
  • C. Kappen
  • Biology, Medicine
    American journal of medical genetics. Part C, Seminars in medical genetics
  • 2013
TLDR
Recent progress toward a better understanding of nutrients during pregnancy is reviewed, with particular focus on mouse models for defective neural tube closure, suggesting that efforts to prevent neural tube defects with nutritional supplementation may need to become more specifically targeted than previously appreciated.
Embryonic defence mechanisms against glucose-dependent oxidative stress require enhanced expression of Alx3 to prevent malformations during diabetic pregnancy
TLDR
ALX3 deficiency provides a novel molecular mechanism for developmental defects arising from maternal hyperglycaemia by stimulating the expression of oxidative stress-scavenging genes in a glucose-dependent manner via Foxo1 activation.
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References

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TLDR
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