Streptozotocin (SZ) treated virgin female rats, classified as either manifest diabetic (MD) or subdiabetic (SD) according to intraperitoneal glucose tolerance tests, were mated. Normal untreated rats (N) were also mated and used as controls. On gestational day 20 the MD foetuses showed decreased litter sizes, elevated blood glucose values and glucose-to-insulin ratios, decreased body and pancreatic weights and markedly diminished pancreatic insulin contents. The MD pregnancy was prolonged by two days and about 50 per cent of the offspring died perinatally. Both the wet and dry carcass weights of the non-viable MD offspring were increased, but when correction was made for the prolonged gestational period both the viable and non-viable newborns were lighter than those of the other groups. In the viable newborns of MD mothers the blood glucose concentration was elevated and the pancreatic contents of insulin and somatostatin decreased while that of glucagon remained unchanged. The 20-day-old SD foetuses showed increased pancreatic insulin and somatostatin contents but were identical to N foetuses in all other respects. Similarly, the newborns of SD mothers remained indistinguishable from those of the N mothers.

It is concluded that, in the rat, severe SZ-diabetes induced before pregnancy causes foetal growth retardation and decreased pancreatic insulin stores. The observations suggest that excessive hyperglycaemia in the foetus hampers the normal development of the pancreatic B-cell. The absence of macrosomia and hyperinsulinism in both the MD and SD newborns suggests a difference between human and rat foetal development in diabetic pregnancy.