Menon R K, Sperling M A
Department of Endocrinology, Children's Hospital Medical Center, Cincinnati, OH 45229.
Semin Perinatol. 1988 Apr;12(2):157-62.
In summary, the surges of glucagon and epinephrine at birth, coupled with the fall in insulin secretion, are in accord with appropriate receptor changes, as well as genetic ontogenic patterns of enzyme development. Enzyme activities are further stimulated by the hormonal changes at birth; phosphorylase is activated by glucagon and epinephrine, while PEPCK is activated by glucagon and its expression is facilitated by the fall in insulin. In concert, these changes permit rapid activation of catabolic processes and the mobilization and utilization of endogenous fuel stores. Glucose homeostasis is maintained by glycogenolysis and gluconeogenesis supported by the appropriate enzyme inductions. The free fatty acids released, via lipolysis, also serve to sustain gluconeogenesis, since hepatic fatty acid oxidation is necessary for gluconeogenesis by providing the essential cofactors. This framework permits a rational interpretation of the mechanisms underlying the remarkable transition from intrauterine dependence on maternal glucose to extrauterine autonomy of newborn energy integration. This framework can also explain several causes of neonatal hypoglycemia and act as a base for future investigations.
