Maternal fuels, diabetic embryopathy: pathomechanisms and prevention.
Congenital malformations remain the major cause of morbidity and mortality among the offspring of women with diabetes. Animal and human studies indicate that these anomalies occur very early in pregnancy and result from derangements of the maternal metabolic fuels which support embryogenesis. The mechanism for induction of dysmorphogenesis in experimental diabetic pregnancy has been shown to include deficiency states of membrane lipids (myoinositol, arachidonic acid, etc.), alteration in the prostaglandin cascade, and the generation of excess free oxygen radicals. These biochemical alterations result in characteristic morphological and molecular changes which are considered to be the basis of diabetic embryopathy. This article not only discusses the pathomechanism, but also reviews both clinical and experimental strategies to prevent diabetes-associated birth defects.
Reece
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EA
Department of Obstetrics, Gynecology and Reproductive Sciences, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.
D000818:Animals; D000013:Congenital Abnormalities / Q000209:etiology* / Q000517:prevention & control; D019587:Dietary Supplements; D004195:Disease Models, Animal; D005260:Female; D005609:Free Radicals / Q000009:adverse effects; D006801:Humans; D006943:Hyperglycemia / Q000503:physiopathology; D015227:Lipid Peroxidation; D008563:Membrane Lipids; D051379:Mice; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000150:complications*; D011295:Prenatal Care; D011453:Prostaglandins / Q000494:pharmacology*; D051381:Rats; D017382:Reactive Oxygen Species
D005609:Free Radicals; D008563:Membrane Lipids; D011453:Prostaglandins; D017382:Reactive Oxygen Species