Journal
BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
Volume 88, Issue 10, Pages 779-790Publisher
WILEY
DOI: 10.1002/bdra.20704
Keywords
diabetic pregnancy; diabetic embryopathy; neural tube defect; cardiac outflow tract defect; hyperglycemia; oxidative stress; Pax3; p53
Categories
Funding
- [RO1 DK52865]
- [RO1 DK58300]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK058300, R01DK052865] Funding Source: NIH RePORTER
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Maternal pregestational diabetes (type 1 or type 2) poses an increased risk for a broad spectrum of birth defects. To our knowledge, this problem first came to the attention of the Teratology Society at the 14th Annual Meeting in Vancouver, B.C. in 1974, with a presentation by Lewis Holmes, Etiologic heterogeneity of neural tube defects. Although advances in the control of diabetes in the decades since the discovery of insulin in the 1920's have reduced the risk for birth defects during diabetic pregnancy, the increasing incidence of diabetes among women of childbearing years indicates that this cause of birth defects is a growing public health concern. Major advances in understanding how a disease of maternal fuel metabolism can interfere with embryogenesis of multiple organ systems have been made in recent years. In this review, we trace the history of the study of diabetic teratogenesis and discuss a model in which tissue-specific developmental control genes are regulated at specific times in embryonic development by glucose metabolism. The major function of such genes is to suppress apoptosis, perhaps to preserve proliferative capability, and inhibit premature senescence. Birth Defects Research (Part A) 88:779-790, 2010. (C) 2010 Wiley-Liss, Inc.
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