The premature deposition or lysis of glycogen in livers of fetal rats injected with hydrocortisone or glucagon

Glycogen deposition in fetal rat liver was produced prematurely and in increased amounts by the administration of hydrocortisone to intact fetuses in utero. Extensive glycogenolysis, like that normally occurring in neonatal livers, was brought about prenatally by the administration of glucagon or dibutyryl cyclic AMP to fetal rats 1-2 days before term. The concomitant rise in the level of glucose-6-phosphatase was not causally related to this process since actinomycin D prevented the rise in the level of this enzyme without preventing glycogenolysis. Large doses of glucagon (or dibutyryl cyclic AMP) injected to pregnant rats did not cause glycogen depletion in the fetal livers indicating that this hormone is not transmitted to the fetal circulation. The results suggest that glucocorticoids secreted by the fetal rat initiate the prenatal deposition of liver glycogen and that glucagon, secreted during the neonatal state of hypoglycemia, causes glycogenolysis in the newborn.