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Diabetes 51:2811-2816, 2002
© 2002 by the American Diabetes Association, Inc.

Maternal Diabetes Increases the Risk of Caudal Regression Caused by Retinoic Acid

Billy W.H. Chan1, Kwok-siu Chan1, Tsuyoshi Koide2, Sau-man Yeung1, Maran B.W. Leung1, Andrew J. Copp3, Mary R. Loeken4, Toshihiko Shiroishi2, and Alisa S.W. Shum1

1 Department of Anatomy, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
2 Mammalian Genetics Laboratory, National Institute of Genetics, Mishima, Japan
3 Neural Development Unit, Institute of Child Health, University College London, London U.K.
4 Section on Cellular and Molecular Physiology and Department of Medicine, Joslin Diabetes Center and Harvard Medical School, Boston, Massachusetts

Maternal diabetes increases the risk of congenital malformations in the offspring of affected pregnancies. This increase arises from the teratogenic effect of the maternal diabetic milieu on the developing embryo, although the mechanism of this action is poorly understood. In the present study, we examined whether the vitamin A metabolite retinoic acid (RA), a common drug with well-known teratogenic properties, may interact with maternal diabetes to alter the incidence of congenital malformations in mice. Our results show that when treated with RA, embryos of diabetic mice are significantly more prone than embryos of nondiabetic mice to develop caudal regression, a defect that is highly associated with diabetic pregnancy in humans. By studying the vestigial tail (Wnt-3avt) mutant, we provide evidence that Wnt-3a, a gene that controls the development of the caudal region, is directly involved in the pathogenic pathway of RA-induced caudal regression. We further show that the molecular basis of the increased susceptibility of embryos of diabetic mice to RA involves enhanced downregulation of Wnt-3a expression. This positive interaction between RA and maternal diabetes may have implications for humans in suggesting increased susceptibility to environmental teratogens during diabetic pregnancy.


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Copyright © 2002 by the American Diabetes Association.