title: [Studies on the fetal and neonatal secretion of glucagon and the development of glucagon receptors].
abstract: In order to clarify the potential roles of glucagon for energy induction during the perinatal period, the developmental changes of serum glucagon concentration, the ontogenesis of hepatic glucagon receptor and glucagon-sensitive adenylate cyclase system were estimated in comparison with insulin in rats. In fetal rats on day 18 to 20 gestation, serum glucose levels and hepatic glycogen contents gradually increased as pregnancy progressed. The levels of serum glucagon and its binding to liver microsomal membranes were significantly lower than in adults, and glucagon-sensitive c-AMP production was also markedly suppressed. On day 21 of gestation, hepatic glycogen contents markedly increased to the maximal level, serum glucagon level increased, and glucagon receptors in the fetal liver were already estimated at the same level as in the adult. However, glucagon-sensitive c-AMP production was still suppressed the same as in the fetuses of earlier gestational ages. On the other hand, serum insulin levels in fetuses were higher than those in adults, and the abundant receptor could also be observed in liver microsomal membranes. After delivery, serum glucose rapidly decreased with a marked decline of hepatic glycogen contents until 5 hours in the neonatal period. Serum glucagon and its hepatic receptors were significantly increased with a gradual development of the glucagon-sensitive adenylate cyclase system. Conversely, serum insulin levels were suppressed without any remarkable change in its receptor. From these results, it is suggested that glucagon plays an important role in the neonatal adaptation mechanism, especially in the production of endogenous glucose in place of the transplacental supply from the mother, such effects of glucagon are already initiated by the induction of its receptor in target tissues in the fetus on late gestation.
authors.affiliation: Department of Obstetrics and Gynecology, Kobe University, School of Medicine, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Fujii
authors.forename: H
authors.initials: H
authors.lastname: Morikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Ueda
authors.forename: M
authors.initials: M
authors.lastname: Mochizuki
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism; D000242:Cyclic AMP / Q000096:biosynthesis; D005260:Female; D005333:Fetus / Q000378:metabolism*; D005934:Glucagon / Q000097:blood*; D008112:Liver Glycogen / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D011919:Rats, Inbred Strains; D011964:Receptors, Gastrointestinal Hormone / Q000096:biosynthesis*; D018027:Receptors, Glucagon
chemical_list: D001786:Blood Glucose; D008112:Liver Glycogen; D011964:Receptors, Gastrointestinal Hormone; D018027:Receptors, Glucagon; D005934:Glucagon; D000242:Cyclic AMP