Congenital malformations and intrauterine growth retardation in streptozotocin induced diabetes during gestation in the rat.

Diabetes was induced in Wistar rats by single intraperitoneal injections of streptozotocin (STZ) (50 mg/kg, in citrate buffer pH 4.7) at both preimplantation and organogenetic stages. The controls were either buffer treated or, following STZ administration, injected intraperitoneally with 2 to 6 IU of insulin daily until term. Fetuses collected on day 20 were found to have several malformations. Major abnormalities included gastroschisis and evisceration, maxillary hypoplasia and interatrial, and interventricular septal defects. Intrauterine growth retardation was present in most of the diabetic groups. Heavier placentae and shorter umbilical cords were also observed. Malformations and intrauterine growth retardation were numerous and severe in the preimplantation treatment groups. Insulin administration significantly improved the fetal body weight but did not change the malformation rate in the group made diabetic during organogenesis. It appears that the duration of hyperglycemic state plays a crucial role in malformation and growth retardation, and meticulous control of blood sugar from early stages has significant beneficial effects on fetal development.