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Related Experiment Videos

Diabetic embryopathy: possible pathogenesis

L S Sadler1, L K Robinson, M E Msall

  • 1Division of Genetics, State University of New York at Buffalo, USA.

American Journal of Medical Genetics
|January 30, 1995
PubMed
Summary
This summary is machine-generated.

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Offspring of diabetic mothers face higher congenital malformation risks. Early diabetic embryopathy may stem from damage to embryonic somite mesoderm and neural crest cells.

Area of Science:

  • Developmental biology
  • Reproductive medicine
  • Teratology

Background:

  • Improved metabolic control in diabetic pregnancy has not eliminated increased congenital malformation risks in offspring.
  • Insulin-dependent diabetic pregnancies carry a 2- to 4-fold higher risk of birth defects.

Purpose of the Study:

  • To investigate the pathogenesis of congenital malformations in offspring of diabetic women.
  • To identify specific embryonic structures potentially affected in diabetic embryopathy.

Main Methods:

  • Evaluation of structural defects in infants born to insulin-dependent diabetic mothers.
  • Review of existing literature on diabetic embryopathy.

Main Results:

  • Four infants of insulin-dependent diabetic mothers exhibited abnormal ears and vertebral defects.

Related Experiment Videos

  • Analysis suggests a potential primary insult to developing somite mesoderm.

    • Conclusions:

    • Diabetic embryopathy may involve damage to embryonic somite mesoderm and cephalic neural crest cells.
    • Early embryonic development, particularly somite and neural crest formation, is vulnerable in diabetic pregnancies.