Smith B T, Tanswell A K, Minshall D, Bogues W N, Vreeken E
Biol Neonate. 1982;42(5-6):201-7. doi: 10.1159/000241600.
Lung and liver glycogen and corticosteroid 11-reductase activity were studied in fetal and neonatal rats. Glycogen content peaked in the lung on day 20 of gestation, while hepatic glycogen content was generally lower and peaked later. Both pre- and postnatally, betamethasone administration resulted in lowered pulmonary and elevated hepatic glycogen. In both lung and liver, corticosteroid 11-reductase activity showed an inverse developmental pattern to glycogen content. Betamethasone elevated pulmonary corticosteroid 11-reductase activity and lowered hepatic activity. In lung and liver, glycogen content and corticosteroid 11-reductase activity are tightly linked during development and following glucocorticoid therapy.
对胎鼠和新生大鼠的肺与肝脏糖原及皮质类固醇11 -还原酶活性进行了研究。糖原含量在妊娠第20天在肺中达到峰值，而肝脏糖原含量通常较低且峰值出现较晚。产前和产后给予倍他米松均导致肺糖原降低而肝糖原升高。在肺和肝脏中，皮质类固醇11 -还原酶活性与糖原含量呈现相反的发育模式。倍他米松提高了肺皮质类固醇11 -还原酶活性并降低了肝脏活性。在肺和肝脏中，糖原含量和皮质类固醇11 -还原酶活性在发育过程中以及糖皮质激素治疗后紧密相关。
