Levitsky L L, Edidin D V, Menella J A, Spaulding N H, Hsieh L C
Biol Neonate. 1986;49(1):36-42. doi: 10.1159/000242507.
Renal and hepatic levels of the rate-limiting gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK) were determined in control and intrauterine growth-retarded rate neonates and dams. Dexamethasone and surgically induced intrauterine growth retardation (IUGR) resulted in an elevation of neonatal renal PEPCK activity, but did not affect hepatic PEPCK levels. In the dam, glucocorticoid administration resulted in an increase in renal PEPCK, but did not affect the hepatic enzyme. We have demonstrated that, unlike the hepatic enzyme, renal PEPCK could potentially contribute to gluconeogenesis in utero, since dexamethasone administration significantly increased renal PEPCK at birth. This study confirms the hypothesis that hepatic and renal PEPCK activities are regulated independently in both the adult and neonatal animal.
在对照及宫内生长受限的新生大鼠及其母鼠中测定了糖异生限速酶磷酸烯醇式丙酮酸羧激酶(PEPCK)的肾脏和肝脏水平。地塞米松及手术诱导的宫内生长受限(IUGR)导致新生大鼠肾脏PEPCK活性升高,但不影响肝脏PEPCK水平。在母鼠中,给予糖皮质激素导致肾脏PEPCK增加,但不影响肝脏中的该酶。我们已经证明,与肝脏中的酶不同,肾脏PEPCK可能在子宫内对糖异生有贡献,因为出生时给予地塞米松可显著增加肾脏PEPCK。本研究证实了在成年和新生动物中,肝脏和肾脏PEPCK活性受到独立调节的假说。