Dietary vitamin E prophylaxis and diabetic embryopathy: Morphologic and biochemical analysis

• Published in: American journal of obstetrics and gynecology 1996-10, Vol.175 (4), p.793-799
• Main Authors: Sivan, Eyal, Reece, E.Albert, Wu, Ying-King, Homko, Carol J., Polansky, Marcia, Borenstein, Michael
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Diabetes; Diabetes Mellitus, Experimental - blood; Diabetes Mellitus, Experimental - complications; Diabetes Mellitus, Experimental - drug therapy; Diet; Diseases of mother, fetus and pregnancy; embryopathy; Female; Fetal Resorption - epidemiology; Fetal Resorption - etiology; Fetal Resorption - prevention & control; free oxygen radicals; Gynecology. Andrology. Obstetrics; Incidence; Insulin - therapeutic use; Medical sciences; Neural Tube Defects - epidemiology; Neural Tube Defects - etiology; Neural Tube Defects - prevention & control; Pregnancy; Pregnancy in Diabetics; Pregnancy. Fetus. Placenta; Rats - embryology; Rats, Sprague-Dawley; Superoxide Dismutase - blood; vitamin E; Vitamin E - administration & dosage; Vitamin E - blood; Vitamin E - therapeutic use
• ISSN: 0002-9378; 1097-6868
• DOI: 10.1016/S0002-9378(96)80001-9

OBJECTIVE: In this study we sought to determine whether dietary supplementation with vitamin E, a known antioxidant, would reduce the incidence of diabetic embryopathy in an in vivo rat model. STUDY DESIGN: Eighty-day-old Sprague-Dawley rats were assigned to one of five groups: two control groups (groups 1 and 2) and three diabetic groups (groups 3, 4, and 5). One group of controls (group 2) and one group of diabetic rats (group 4) received dietary supplements of vitamin E (440 mg/day). The other three groups (groups 1, 3, and 5) received a normal diet only. Group 5 received insulin therapy to control glucose levels. On day 6 of gestation diabetes was induced in groups 3, 4, and 5 with streptozotocin (65 mg/kg). Animals were killed on day 12; embryos were examined for size, protein content, evidence of malformations, and superoxide dismutase activity. RESULTS: In both groups (groups 3 and 4) of diabetic rats the mean blood glucose level than was significantly higher in controls. Insulin-treated animals (group 5) had glucose levels that were comparable to those of controls. The unsupplemented diabetic group had a neural tube defect rate of 21.48% ± 9.6% (percentage of neural tube defects per rat) and a resorption rate of 21.37% ± 20.39% (percentage of resorptions per rat) as compared with rates in the supplemented diabetic group of 6.92% ± 4.08% and 2.17% ± 3.74%, respectively (p < 0.01). Groups 1, 2, and 5 had similar neural tube defect rates (6.63% ± 5.0%, 5.01% ± 4.87%, and 3.55% ± 5.92%, respectively. Vitamin E levels, measured by high-performance liquid chromatography, were significantly higher in maternal serum and embryos in the supplemented groups (p < 0.001) than in controls. Superoxide dismutase activity was reduced in the diabetes groups and was not affected by vitamin E therapy. CONCLUSIONS: Supplementation with the antioxidant vitamin E confers a significant protective effect against diabetic embryopathy and may potentially serve as a dietary prophylaxis in the future. We postulate that this protective effect is mediated by a reduction in the oxidative load induced by hyperglycemia. (Am J Obstet Gynecol 1996;175:793-9.)