RT Book, Section A1 Rozance, Paul J. A1 Hay, Jr., William W. A1 Wright, Clyde J. A2 Kline, Mark W. SR Print(0) ID 1182920471 T1 Disorders of Glucose, Electrolytes, and Acid–Base Balance T2 Rudolph's Pediatrics, 23e YR 2018 FD 2018 PB McGraw-Hill Education PP New York, NY SN 9781259588594 LK accesspediatrics.mhmedical.com/content.aspx?aid=1182920471 RD 2024/03/28 AB Normal postnatal glucose homeostasis is established by increased glucose production and utilization. Factors that promote glucose production include catecholamines and glucagon, which activate glycogenolysis. A high glucagon-to-insulin ratio, which induces synthesis and activity of the enzymes, is required for there to be gluconeogenesis. Once normal feedings are established, glycerol and amino acids continue to fuel gluconeogenesis while dietary fatty acids activate the enzymes responsible for gluconeogenesis. Additionally, galactose derived from the hydrolysis of milk sugar (lactose) in the gut increases hepatic glycogen production for sustained between-feeding hepatic glucose release from glycogen breakdown. Feeding also induces production of intestinal peptides, or incretins, that promote insulin secretion. Insulin decreases hepatic glucose production and increases glucose utilization for energy production and storage as glycogen. These opposing conditions of glucose production and utilization continue in response to normal feed-fast cycles, regulating normal plasma glucose concentrations.