Intermittent hypoglycemia was produced in normal pregnant rats by the administration of 0.5 I.U. of Protamine Zinc Insulin at twelve-hour intervals during either the last two weeks or the final week of pregnancy. The animals treated during the final week of pregnancy delivered significantly lighter litters, with a reduction in the weight of the living pups, and with a significant increase in the incidence of stillbirths which were significantly lighter than the pups delivered to the untreated controls. The exact cause of the growth retardation and the excessive loss are as yet unknown. Two alternate hypotheses are suggested: (1) that growth retardation occurred as the result of relative inanition of the fetus associated with the maternal hypoglycemia, less carbohydrate being available for fetal nutrition and growth, or (2) that with intermittent hypoglycemia there was less stimulation of the fetal pancreatic islets and of the production of insulin with its growth-promoting properties.
The animals treated with insulin for the last two weeks of pregnancy delivered litters of equal number and weight as the controls; the living pups were of equal weight compared to the controls; the number and weight of the stillborn pups was significantly increased. To explain this unexpected finding, it is suggested that in time adrenal cortical hyperfunction occurs secondary to intermittent bouts of hypoglycemia and that the normal or excessive growth is the result of excessive amounts of maternal adrenal corticoids.
