Metabolic Fuels in the Embryo and the Newborn

Abstract

Although insulin and glucagon can be detected on the 11th day of gestation in the rat fetal pancreas, the secretion and biologic action of these hormones do not reach maturity until after the 30th day of postnatal life. During the perinatal life, the B and A cells are relatively insensitive to glucose, glucose tolerance is abnormal and the insulinogenic response to glucose is decreased. In spite of this, the hypersecretion of insulin by the fetal pancreas during the last days of pregnancy and the increased glucagon release immediately after birth, favor the storage and subsequent mobilization of nutrient. Although glucagon inhibits anabolic processes, such as the synthesis of hepatic DNA and the deposition of hepatic glycogen and although in the fetus these processes proceed at an extremely rapid rate, the concentration of plasma glucagon on the 21st day of fetal life is as high as it is in the adult rat. This apparent paradox can be explained by the delayed development of the hepatocyte glucagon receptors and therefore of the adenylate cyclase response to this hormone. On the 15th day of fetal life,the binding of I125- glucagon by liver membranes was only 1% of the adult level, increased to 23% by the 21st day, but like the adenylate cyclase response to glucagon, did not reach maturity until after the 30th day of postnatal life.