Key result
While overall congenital heart defect rates did not differ significantly, ovarian stimulation in severely hyperglycemic mice (>400 mg/dL) significantly increased fetal cardiac malformations compared to non-stimulated controls (61% vs 27%, p=0.04).
Why the study?
The study was conducted to examine the incidence of congenital heart defects in offspring born to hyperglycemic mothers with and without ovarian stimulation.
Does ovarian stimulation increase the incidence of congenital heart defects in offspring of severely hyperglycemic mice?
Does ovarian stimulation increase the incidence of congenital heart defects in offspring of severely hyperglycemic mice?
In a murine model, ovarian stimulation in the setting of severe maternal hyperglycemia (>400 mg/dL) significantly increased the incidence of fetal congenital heart defects.
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.
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Lister et al. (2019) studied Maternal hyperglycemia (n=99). Ovarian stimulation (pregnant mare serum and human chorionic gonadotropin) vs. Non-stimulated hyperglycemic dams was evaluated on Incidence of congenital heart defects (CHD) in progeny (p=0.14). While overall congenital heart defect rates did not differ significantly, ovarian stimulation in severely hyperglycemic mice (>400 mg/dL) significantly increased fetal cardiac malformations compared to non-stimulated controls (61% vs 27%, p=0.04).
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