Hormonal Control of Liver Glycogen in Fetal and Newborn Rats

Liver glycogen in the rat was much accumulated in the end of the fetal life, followed by a marked decrease just after birth. Decapitation of a fetus caused a retardation of storage of glycogen in its liver, and this retardation was prevented totally by the administration of cortisone acetate and partially by that of ACTH to the decapitated fetus. Concomitant maternal adrenalectomy and fetal decapitation caused a striking decrease of glycogen in the fetal liver. These observations suggest that both the fetal hypophyseal adrenal system and the maternal adrenal play an important role in the glycogen storage in the fetal liver. Following the injection of ACTH or cortisone acetate to the newborn rats, the liver glycogen was much accumulated. These results obtained in fetuses and newborns support the view that the marked loss of glycogen in the neonatal liver may be resulted in part by a decline of hormonal support which is a decline of the neonatal hypophyseal adrenal activity and the cessation of supply of maternal corticoids