Diabetes in pregnancy: experimental aspects.
Substantial literature indicates that diabetes in pregnant rats and mice induces embryo lethality, growth retardation, and a variable incidence of birth defects. All these embryopathic effects appear to be mediated by several factors, e.g. genetic disposition and the composition of the diets eaten by the animals. Studies carried out on rodent embryos cultured in vitro showed that numerous components of the diabetic state (ketone bodies, somatomedin inhibitors, low concentrations of insulin) display a dysmorphogenic potential. Besides, diabetes-induced malformations have been often related, both in vivo and in vitro studies, to morphological and physiological alterations of the yolk sac, the principal organ for the passage of nutrients from the mother to the rodent embryo. On the whole, in vivo and in vitro experiments indicate that hyperglycemia itself is not a major factor in producing diabetic embryopathies that are more likely ascribable to severe alterations of the embryonic energetic balance.
Giavini
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Dipartimento di Biologia, Università degli Studi, Milan, Italy.
D000818:Animals; D001786:Blood Glucose; D000013:Congenital Abnormalities / Q000209:etiology* / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology; D004032:Diet; D004734:Energy Metabolism; D005260:Female; D005315:Fetal Diseases / Q000209:etiology* / Q000378:metabolism; D005327:Fetal Resorption / Q000209:etiology; D008297:Male; D051379:Mice; D009924:Organ Culture Techniques; D010920:Placenta / Q000098:blood supply; D011247:Pregnancy; D011256:Pregnancy Outcome; D011254:Pregnancy in Diabetics / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013045:Species Specificity; D015017:Yolk Sac / Q000378:metabolism
D001786:Blood Glucose