Fetal hyperglycemia and hyperinsulinemia, as induced by administration of streptozotocin to pregnant rats, during late gestation resulted in the onset of the major period of hepatic glycogen synthesis and accumulation at days 19-20 of gestation (22 days = term) rather than at days 20-21, as for normal fetuses. In addition, sustained high levels of liver synthase phosphatase and phosphorylase phosphatase activities prevented the normal term increase in activation of phosphorylase and inactivation of synthase in hyperglycemic/hyperinsulinemic fetuses. The suppression of term fetal changes in phosphorylase activation in particular contributed to the maintenance at term of fetal liver in a condition favoring glycogenesis rather than glycogenolysis.
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