Effects of sera from Cohen, genetically determined diabetic rats, streptozotocin diabetic rats and sucrose fed rats on in vitro development of early somite rat embryos

The effects of sera from genetically determined Cohen diabetic rats, streptozotocin (STZ) diabetic rats and non-diabetic control rats fed a 72% sucrose diet on the in vitro development of 9 1/2 day old rat embryos from control rats have been studied. Hyperglycemic sera from diabetic rats had a high teratogenic effect: abnormalities were seen in 41.5% of embryos cultured in serum from Cohen diabetic animals and in 54% of embryos cultured in serum from STZ-diabetic rats. Malformations were seen in 25-27% of embryos cultured in serum from 2 groups of control rats fed a high sucrose diet compared with 10.7% in serum from control rats maintained on regular diet. When embryos from the experimental groups were cultured in serum from control rats on regular diet malformations were seen in 24.7% of embryos from Cohen genetically determined diabetic rats vs 10.9-12.4% in embryos from 2 non-diabetic groups. Only 14% of embryos from STZ-diabetic rats exhibited malformations when cultured in the control serum, but 42% of embryos from the same rats showed abnormalities when grown in serum from STZ-diabetic rats. Normalization of glucose level in the serum of STZ-diabetic rats by prior injection of insulin did not reduce the high incidence of malformations (51%). The high rate of embryonic malformations correlated with the ultrastructural changes of their visceral yolk sac endoderm. We suggest that serum from diabetic rats is teratogenic even at moderate hyperglycemia. Malformations in embryos derived from STZ-diabetic rats may be partially prevented by culturing in normoglycemic control serum, but not in embryos from Cohen diabetic rats, implying a genetic predisposition in these embryos to the development of congenital malformations.