Lebenthal E
Pediatr Res. 1977 Apr;11(4):282-5. doi: 10.1203/00006450-197704000-00004.
Enterokinase activity is first detected in the small intestine of the rat at the 20th day of gestation, whereas sucrase activity first appears in the 14th day of postnatal life. Intraperitoneal injection of hydrocortisone to pregnant rats before the normal appearance of enterokinase in fetuses causes the premature appearance of enterokinase (58 +/- 8 units), but not of sucrase activity. The addition of actinomycin D in the pregnant rat results in supermaximal stimulation of enterokinase activity (229 +/- 25 units). Sucrase activity is stimulated by hydrocortisone when given in the first 3 days of life (118 +/- 0.04 units). The maximal induction occurs 2 days before the normal appearance of the enzyme in untreated animals (7.3 +/- 12 units). The addition of actinomycin D diminished the effect of hydrocortisone on sucrase activity in the neonatal rat (1.4 +/- 2 units versus 1.8 +/- 0.4 units in 3-day-old rats). Thus, enterokinase and sucrase of the small intestine of the fetal and infant rat respond differently to combined hydrocortisone and actinomycin D. The response to hydrocortisone is age dependent and the maximal induction occurs before the time of the natural appearance of the enzymes. No effect is elicited after the normal appearance of enterokinase or sucrase. Glucocoticoids stimulate an early appearance of small intestinal enzymes only before the expected time of the natural development burst of activity. In both, sucrase and enterokinase, glucocorticoids have no effect after the enzymes are fully developed. New enzymes develop in clusters during the late fetal, neonatal, and late sucking periods. The effect of glucocorticoids on the "maturation" of the small intestine is limited to the induction of one phase only; i.e., only before the late fetal period is the precocious appearance of enterokinase possible. The induction of enterokinase activity can serve as an indicator for the early phase of maturation. Whereas the induction of sucrase activity can serve as a marker for late phase of maturation of the small intestine in the rat. The superinduction of enterokinase, but not of sucrase activity, by the addition of actinomycin D to glucocorticoids might be related to the different stability of the mRNA's of these enzymes.
肠激酶活性在妊娠第20天首次在大鼠小肠中被检测到，而蔗糖酶活性在出生后第14天首次出现。在胎儿正常出现肠激酶之前，给怀孕大鼠腹腔注射氢化可的松会导致肠激酶提前出现（58±8单位），但不会导致蔗糖酶活性提前出现。在怀孕大鼠中添加放线菌素D会导致肠激酶活性的超最大刺激（229±25单位）。在出生后的前3天给予氢化可的松可刺激蔗糖酶活性（118±0.04单位）。最大诱导出现在未处理动物中该酶正常出现前2天（7.3±12单位）。添加放线菌素D会减弱氢化可的松对新生大鼠蔗糖酶活性的影响（1.4±2单位，而3日龄大鼠为1.8±0.4单位）。因此，胎儿和婴儿大鼠小肠中的肠激酶和蔗糖酶对氢化可的松和放线菌素D的联合反应不同。对氢化可的松的反应具有年龄依赖性，最大诱导出现在酶自然出现的时间之前。肠激酶或蔗糖酶正常出现后没有影响。糖皮质激素仅在预期的自然活性爆发时间之前刺激小肠酶的早期出现。在蔗糖酶和肠激酶中，酶完全发育后糖皮质激素均无作用。新酶在胎儿后期、新生儿期和晚期吸吮期成簇发育。糖皮质激素对小肠“成熟”的影响仅限于诱导一个阶段；即，只有在胎儿后期之前，肠激酶才可能提前出现。肠激酶活性的诱导可作为成熟早期阶段的指标。而蔗糖酶活性的诱导可作为大鼠小肠成熟后期阶段的标志物。在糖皮质激素中添加放线菌素D对肠激酶的超诱导作用，而非对蔗糖酶活性的超诱导作用，可能与这些酶mRNA的不同稳定性有关。
