Li J, Saunders J C, Gilmour R S, Silver M, Fowden A L
Department of Cellular Physiology, Institute of Animal Physiology and Genetics Research, Babraham, Cambridge, United Kingdom.
Endocrinology. 1993 May;132(5):2083-9. doi: 10.1210/endo.132.5.8477658.
Using RNase protection analysis, insulin-like growth factor-II (IGF-II) mRNA levels were measured in various tissues from fetal sheep during late gestation (term, 146 +/- 2 days) and after experimental manipulation of fetal plasma cortisol levels. No gestational trend in IGF-II mRNA levels was observed in the fetal lung, kidney, or skeletal muscle. However, in the fetal liver, there was a marked decline in IGF-II mRNA abundance immediately before term, which closely paralleled the normal prepartum surge in fetal plasma cortisol. This decrease in hepatic IGF-II mRNA levels toward term was prevented when the cortisol surge was abolished by fetal adrenalectomy and was stimulated prematurely in fetuses younger than 130 days by exogenous infusion of cortisol. Hepatic and renal IGF-II mRNA abundances were also reduced when fetal cortisol levels were raised endogenously by maternal fasting in late gestation. Muscle IGF-II mRNA levels were reduced by fetal cortisol infusion, but not by maternal fasting, and were higher in adrenalectomized than in intact fetuses in late gestation. No change in IGF-II mRNA levels were observed in the fetal lung in response to altering the fetal cortisol level either exogenously or endogenously. When the data from all fetuses were combined regardless of treatment or gestational age, there was a significant inverse correlation between the plasma cortisol level in utero and IGF-II mRNA abundance in the fetal liver (P < 0.001), but not in any of the other fetal tissues studied. These findings show that cortisol suppresses IGF-II gene expression in the liver of the sheep fetus and indicate that the developmental change in hepatic IGF status toward term may be due to the prepartum cortisol surge.
采用核糖核酸酶保护分析法，检测了妊娠晚期（足月，146±2天）绵羊胎儿各组织中胰岛素样生长因子-II（IGF-II）mRNA水平，并在实验性改变胎儿血浆皮质醇水平后进行了检测。在胎儿肺、肾或骨骼肌中未观察到IGF-II mRNA水平的妊娠趋势。然而，在胎儿肝脏中，足月前IGF-II mRNA丰度显著下降，这与胎儿血浆皮质醇正常的产前激增密切平行。当通过胎儿肾上腺切除术消除皮质醇激增时，足月时肝脏IGF-II mRNA水平的这种下降得到了预防，而在130天以下的胎儿中，通过外源性注入皮质醇可提前刺激这种下降。当妊娠晚期母体禁食使胎儿皮质醇水平内源性升高时，肝脏和肾脏的IGF-II mRNA丰度也会降低。胎儿注入皮质醇可降低肌肉IGF-II mRNA水平，但母体禁食则不会，且妊娠晚期肾上腺切除胎儿的肌肉IGF-II mRNA水平高于完整胎儿。无论外源性还是内源性改变胎儿皮质醇水平，胎儿肺中的IGF-II mRNA水平均未观察到变化。当将所有胎儿的数据合并，而不考虑治疗或胎龄时，子宫内血浆皮质醇水平与胎儿肝脏中IGF-II mRNA丰度之间存在显著的负相关（P<0.001），但在其他任何研究的胎儿组织中均未观察到这种相关性。这些发现表明，皮质醇抑制绵羊胎儿肝脏中IGF-II基因的表达，并表明足月时肝脏IGF状态的发育变化可能是由于产前皮质醇激增所致。
