Rolanda Lister1, Etoi Garrison1, Francine Hughes2, Scott Baldwin3, Bin Zhou4. 1. Vanderbilt University Medical Center, Department of Obstetrics and Gynecology, B-1100 Medical Center North, TN, US. 2. New York University, Department of Obstetrics and Gynecology, 150 East 32nd Street, New York, NY, US. 3. Vanderbilt University Medical Center, Department of Pediatrics, 2200 Children's Way, 5230 Doctors' Office Tower, TN, US. 4. Albert Einstein College of Medicine, Department of Pediatrics, Department of Genetics, Department of Medicine, Michael F. Price Center, 1301 Morris Park Avenue, NY, US.
Abstract
OBJECTIVES: To study the incidence of congenital heart defects (CHD) in offspring born to hyperglycemic mothers with and without ovarian stimulation. DESIGN: Reproductive biology. SETTING: Mouse model. PATIENTS: N/A. INTERVENTION: Hyperglycemia was induced in CD-1 wild type female mice using a single intraperitoneal dose of 150 mg/kg of streptozotocin. Stimulated dams (SD); (n=3) were injected with pregnant mare serum and human chorionic gonadotropin 48 hours apart. Non-stimulated dams (NSD); (n=4) were not injected. Both groups were mated with normal male CD-1 mice for timed pregnancies. Fetal hearts were extracted on embryonic day 16.5 and histological analyses was performed. Student's t-tests were employed to compare the incidence of cardiac defects in the SD and NSD groups. P ≤ 0.05 was significant. MAIN UUTCOME MEASURE: The incidence of CHD in progeny of diabetic dams with and without ovarian hyperstimulation. RESULTS & CONCLUSIONS: The average litter size was higher in SD compared to NSD. The average blood glucose for the SD and NSD was similar. Overall, the incidence of cardiac malformations did not differ between the two groups. However, in severe maternal hyperglycemia (>400 mg/dL), there was a higher incidence of fetal cardiac malformations in the pups born to SD vs NSD.
OBJECTIVES: To study the incidence of congenital heart defects (CHD) in offspring born to hyperglycemic mothers with and without ovarian stimulation. DESIGN: Reproductive biology. SETTING: Mouse model. PATIENTS: N/A. INTERVENTION: Hyperglycemia was induced in CD-1 wild type female mice using a single intraperitoneal dose of 150 mg/kg of streptozotocin. Stimulated dams (SD); (n=3) were injected with pregnant mare serum and human chorionic gonadotropin 48 hours apart. Non-stimulated dams (NSD); (n=4) were not injected. Both groups were mated with normal male CD-1 mice for timed pregnancies. Fetal hearts were extracted on embryonic day 16.5 and histological analyses was performed. Student's t-tests were employed to compare the incidence of cardiac defects in the SD and NSD groups. P ≤ 0.05 was significant. MAIN UUTCOME MEASURE: The incidence of CHD in progeny of diabetic dams with and without ovarian hyperstimulation. RESULTS & CONCLUSIONS: The average litter size was higher in SD compared to NSD. The average blood glucose for the SD and NSD was similar. Overall, the incidence of cardiac malformations did not differ between the two groups. However, in severe maternal hyperglycemia (>400 mg/dL), there was a higher incidence of fetal cardiac malformations in the pups born to SD vs NSD.
Entities:
Keywords:
Congenital heart defects; Human chorionic gonadotropin; Hyperglycemia; Ovarian stimulation; Pregnant mare serum
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