Synchronization of the factors critical for diabetic teratogenesis: An in vitro model

• Published in: American journal of obstetrics and gynecology 1996-04, Vol.174 (4), p.1284-1288
• Main Authors: Reece, E.Albert, Wiznitzer, Arnon, Homko, Carol J., Hagay, Zion, Wu, Ying King
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Blood Glucose - metabolism; Congenital Abnormalities - etiology; Diabetes Mellitus, Experimental - blood; Diabetes Mellitus, Experimental - complications; Diabetic embryopathy; Diseases of mother, fetus and pregnancy; Female; Gynecology. Andrology. Obstetrics; Heart Defects, Congenital - etiology; Medical sciences; Neural Tube Defects - etiology; Pregnancy; Pregnancy. Fetus. Placenta; rat embryo culture; Rats; Rats, Sprague-Dawley
• ISSN: 0002-9378; 1097-6868
• DOI: 10.1016/S0002-9378(96)70672-5

OBJECTIVE: Our goal was to determine the relationship between critical factors and conditions such as gestational age and exposure time to elevated glucose levels in diabetic embryopathy. STUDY DESIGN: A postimplantation rat embryo culture was used as a model for investigation. The effect of various factors on embryonic development was studied. Experiments were conducted with increasing glucose concentrations (150 to 905 mg/dl, n = 186), at various gestational ages (10 to 12 days, n = 169), and for varying durations of exposure (30 to 180 minutes, n = 169). Gross morphologic characteristics of the yolk sac and embryo were assessed. RESULTS: Embryopathy was induced by hyperglycemia in a dose-related fashion: a 20% rate at two times control glucose concentration, almost a 50% rate at four times control, and approximately a 100% abnormality rate at more than six times control. A critical window in gestational age, days 10 to 11, and a minimum exposure time to hyperglycemia of 2 hours were necessary to induce teratogenesis. CONCLUSIONS: Diabetic teratogenesis occurs in a dose-related fashion and requires a minimum exposure time and critical gestational age. Only synchronization of these critical conditions induces embryonic maldevelopment. Furthermore, nonsynchronized aberrant conditions may result in apparently normal embryonic development. (AM J OBSTET GYNECOL 1996;174:1284-8.)