Grant support for this paper was RO1 DK52865, RO1 DK58300 (to M.R.L.).
Understanding diabetic teratogenesis: Where are we now and where are we going?†
Article first published online: 12 AUG 2010
Copyright © 2010 Wiley-Liss, Inc.
Birth Defects Research Part A: Clinical and Molecular Teratology
Special Issue: 50th Anniversary of the Teratology Society
Volume 88, Issue 10, pages 779–790, October 2010
How to Cite
Zabihi, S. and Loeken, M. R. (2010), Understanding diabetic teratogenesis: Where are we now and where are we going?. Birth Defects Research Part A: Clinical and Molecular Teratology, 88: 779–790. doi: 10.1002/bdra.20704
- Issue published online: 13 OCT 2010
- Article first published online: 12 AUG 2010
- Manuscript Accepted: 28 MAY 2010
- Manuscript Revised: 20 MAY 2010
- Manuscript Received: 4 APR 2010
- diabetic pregnancy;
- diabetic embryopathy;
- neural tube defect;
- cardiac outflow tract defect;
- oxidative stress;
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), 2010. © 2010 Wiley-Liss, Inc.