Wehrenberg W B, Janowski B A, Piering A W, Culler F, Jones K L
Department of Health Sciences, University of Wisconsin-Milwaukee 53201.
Endocrinology. 1990 Jun;126(6):3200-3. doi: 10.1210/endo-126-6-3200.
Excessive glucocorticoid concentrations are well recognized inhibitors of linear growth, due in part to their suppression of GH secretion. The mechanism of this inhibition has been unclear, especially since glucocorticoids enhance the in vitro GH response of pituitary cells to GH-releasing hormone (GHRH). We investigated the possibility that hypothalamic somatostatin might be mediating these dichotomous observations by using passive immunization techniques. The GH response to GHRH was significantly blunted in rats pretreated with the synthetic glucocorticoid, dexamethasone, compared to that in normal animals. In marked contrast, the immunoneutralization of somatostatin resulted in a significantly enhanced GH response to GHRH in dexamethasone-treated animals. These results suggest that the previously described inhibitory action of glucocorticoids on GH secretion in vivo are mediated via altered hypothalamic somatostatin tone.
糖皮质激素浓度过高是公认的线性生长抑制剂,部分原因在于其对生长激素(GH)分泌的抑制作用。这种抑制作用的机制尚不清楚,特别是因为糖皮质激素可增强垂体细胞在体外对生长激素释放激素(GHRH)的生长激素反应。我们通过被动免疫技术研究了下丘脑生长抑素可能介导这些矛盾观察结果的可能性。与正常动物相比,用合成糖皮质激素地塞米松预处理的大鼠对GHRH的生长激素反应明显减弱。与之形成鲜明对比的是,生长抑素的免疫中和导致地塞米松处理的动物对GHRH的生长激素反应显著增强。这些结果表明,先前描述的糖皮质激素在体内对生长激素分泌的抑制作用是通过下丘脑生长抑素张力的改变介导的。