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Experimental Mechanisms of Diabetic Embryopathy and Strategies for Developing Therapeutic Interventions

Department of Obstetrics and Gynecology; Arkansas Center for birth Defects Research and Prevention, the Department of Pediatrics, The College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas

E. Albert Reece, Md, PhD, MBA

Department of Obstetrics and Gynecology; Arkansas Center for birth Defects Research and Prevention, the Department of Pediatrics, The College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas; reeceealbert{at}uams.edu

A high frequency of birth defects is seen in infants bom to diabetic mothers. The mechanisms by which maternal hyperglycemia, the major teratogenic factor, induces embryonic malformations remain to be addressed. It has been shown that increases in programmed cell death are one of the factors causing embryonic malformations. Hyperglycemia-induced apoptosis is associated with oxidative stress, lipid peroxidation, and decreased antioxidant defense capacity in the embryos. Recent studies have revealed that mitogen-activated protein kinases as intracellular signaling factors are involved in hyperglycemia-induced embryopathy. Based on the findings, interventions to prevent embryonic malformations have been explored. Strategies include supplementation of molecules that are deficient in the embryos under hyperglycemic conditions and antioxidants to alleviate the adverse effects of oxidative stress. The ultimate goal is to develop multi-nutrient dietary supplements to eliminate embryonic abnormalities induced by maternal diabetes.

Key Words: Diabetes • hyperglycemia • embryopathy • birth defect • malformation • apoptosis • oxidative stress • lipid peroxidation • protein kinase C • mitogen-activated protein kinase • antioxidant • intervention

Journal of the Society for Gynecologic Investigation, Vol. 12, No. 8, 549-557 (2005)
DOI: 10.1016/j.jsgi.2005.07.005


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