Gautier C, Habechi Z, Belbekouche M, Vaillant R
Biol Neonate. 1985;48(5):285-91. doi: 10.1159/000242182.
The effects of corticosteroids and pancreatic hormones on two mitochondrial enzymes of ureagenesis, carbamyl phosphate synthetase-I (CPS-I) and ornithine transcarbamylase (OTC), were investigated and compared in fetal rat liver. Supplementing hydrocortisone acetate (50 micrograms) to 18.5-day-old fetuses significantly increased CPS-I activity (by 36%) and decreased OTC activity (by 23%). An actinomycin D supply (2 micrograms) to 18.5-day-old fetuses prematurely increased OTC activity and decreased fetal insulin level (by 42%). This treatment had no effect on CPS-I activity. Glucagon supply (25 micrograms) during the late fetal period increased both activities within 2 h, while dibutyryl-cAMP enhanced OTC activity 17 h later. These results suggested that the fetal development of CPS-I activity was under the control of corticosteroids and glucagon. In contrast, corticosteroid hormones produced an inhibitory effect on OTC activity. This might be explained by the permissive effect of corticosteroids on insulin action, since insulin might act as a repressor in utero of enzyme development. Thus, the paradoxical effect of actinomycin D on OTC activity was probably due to the decrease in fetal insulinemia.
在胎鼠肝脏中研究并比较了皮质类固醇和胰腺激素对尿素生成的两种线粒体酶，即氨甲酰磷酸合成酶-I（CPS-I）和鸟氨酸转氨甲酰酶（OTC）的影响。给18.5日龄胎儿补充醋酸氢化可的松（50微克）可显著增加CPS-I活性（增加36%）并降低OTC活性（降低23%）。给18.5日龄胎儿供应放线菌素D（2微克）可过早增加OTC活性并降低胎儿胰岛素水平（降低42%）。该处理对CPS-I活性无影响。在胎儿后期供应胰高血糖素（25微克）可在2小时内增加两种酶的活性，而二丁酰环磷腺苷在17小时后增强了OTC活性。这些结果表明，CPS-I活性的胎儿发育受皮质类固醇和胰高血糖素的控制。相反，皮质类固醇激素对OTC活性产生抑制作用。这可能是由于皮质类固醇对胰岛素作用的允许效应，因为胰岛素可能在子宫内作为酶发育的抑制剂。因此，放线菌素D对OTC活性的矛盾效应可能是由于胎儿胰岛素血症的降低。
