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Hypoglycemia in the newborn growth-retarded rat: delayed phosphoenolpyruvate carboxykinase induction despite increased glucagon availability.

We have characterized the sequential changes in plasma glucose, insulin and glucagon concentrations, and hepatic glycogen and phosphoenolpyruvate carboxykinase (PEPCK) during the first 240 min of life in rat pups growth retarded [small for gestational age (SGA)] due to bilateral maternal uterine artery ligation. Pups of sham and nonoperated (normal) mothers served as controls. SGA pups were smaller, had reduced liver mass, and demonstrated a pattern of hypoglycemia. They had significantly reduced plasma glucose concentrations at birth, 20, and 240 min but had normal values at 60 and 120 min. SGA pups had significantly reduced hepatic glycogen stores at birth. Plasma glucagon concentrations in SGA pups increased significantly at 20 and 60 min while insulin concentrations decreased equally in all groups. Hepatic PEPCK activity increased greatly in the sham and normal pups. SGA pups did not induce PEPCK during the first 240 min of life; however, pharmacologic doses of glucagon at birth accelerated PEPCK induction in SGA pups and prevented hypoglycemia. These data indicate that newborn SGA pups develop hypoglycemia because of limited hepatic glycogen stores and retarded gluconeogenesis. The delay in PEPCK induction in SGA pups may result from an inadequate although increased glucagon release at birth or diminished sensitivity to available glucagon.