Husson A, Guechairi M, Fairand A, Bouazza M, Ktorza A, Vaillant R
Endocrinology. 1986 Sep;119(3):1171-7. doi: 10.1210/endo-119-3-1171.
The activity changes of two urea cycle enzymes, argininosuccinate synthetase (ASS) and argininosuccinase (ASL), were followed after corticosteroid and pancreatic hormone treatments in utero and in primary cultured fetal hepatocytes. The ASL activity which was induced by glucagon or by (Bu)2cAMP administration was enhanced by a treatment with streptozotocin for 2 days, although ASS was not changed under these conditions. The activity of both enzymes was enhanced by cortisol administration in utero only in streptozotocin-treated fetuses, suggesting an inhibitory effect of insulin. In cultured fetal hepatocytes, dexamethasone produced a marked increase of the two enzyme activities, which was abolished by the simultaneous addition of insulin. The parallel results obtained with these two experimental models allow one to conclude that the high plasma insulin level in late gestation might repress the development of ASS and ASL activities in utero and antagonize the effect of corticosteroids on these enzyme activities.
在子宫内以及原代培养的胎儿肝细胞中，给予皮质类固醇和胰腺激素处理后，对两种尿素循环酶——精氨琥珀酸合成酶（ASS）和精氨琥珀酸酶（ASL）的活性变化进行了追踪研究。用链脲佐菌素处理2天，可增强由胰高血糖素或（Bu）2cAMP诱导的ASL活性，尽管在此条件下ASS活性未发生变化。仅在经链脲佐菌素处理的胎儿中，子宫内给予皮质醇可增强这两种酶的活性，提示胰岛素具有抑制作用。在培养的胎儿肝细胞中，地塞米松可使这两种酶的活性显著增加，但同时添加胰岛素可消除这种增加。这两个实验模型获得的平行结果使人们得出结论，妊娠晚期的高血浆胰岛素水平可能会抑制子宫内ASS和ASL活性的发育，并拮抗皮质类固醇对这些酶活性的影响。
