Klepac R
Exp Clin Endocrinol. 1985 Dec;86(3):305-9. doi: 10.1055/s-0029-1210502.
Glycogen deposition was determined in pregnant rats and their fetuses twenty four hrs after maternal treatment with dexamethasone in the final days of pregnancy. Dexamethasone increases glycogen accumulation in the fetal liver, heart, adrenal glands and thymus. Simultaneously, it increases the glycogen concentration in maternal liver. In this study, dexamethasone did not change the glycogen level in the fetal kidneys, brain, placenta, lung and maternal adrenal glands. These results show that dexamethasone accelerated glycogen deposition in some fetal tissues. It is possible that dexamethasone activated enzymes of glycogen synthesis or potentiated the action of fetal corticosterone on induction of glycogen accumulation in fetal rat tissues.
在孕期最后几天用 dexamethasone 对孕鼠进行母体处理后 24 小时，测定孕鼠及其胎儿的糖原沉积情况。Dexamethasone 可增加胎儿肝脏、心脏、肾上腺和胸腺中的糖原积累。同时，它还会增加母体肝脏中的糖原浓度。在本研究中，dexamethasone 并未改变胎儿肾脏、大脑、胎盘、肺以及母体肾上腺中的糖原水平。这些结果表明，dexamethasone 加速了某些胎儿组织中的糖原沉积。有可能是 dexamethasone 激活了糖原合成酶，或者增强了胎儿皮质酮对诱导胎鼠组织中糖原积累的作用。
