Margolis R N, Seminara D
Department of Anatomy, Howard University, Washington, D.C.
Biol Neonate. 1988;54(3):133-43. doi: 10.1159/000242844.
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.
给妊娠晚期的大鼠注射链脲佐菌素所诱导的胎儿高血糖和高胰岛素血症，导致在妊娠第19 - 20天（22天为足月）而非正常胎儿的第20 - 21天开始肝脏糖原合成和积累的主要阶段。此外，肝脏合酶磷酸酶和磷酸化酶磷酸酶活性持续处于高水平，阻止了高血糖/高胰岛素血症胎儿在足月时磷酸化酶激活和合酶失活的正常增加。尤其是对足月胎儿磷酸化酶激活变化的抑制，有助于使足月时胎儿肝脏维持在有利于糖原生成而非糖原分解的状态。
