Parthasarathy Chandrakesan, Balasubramanian Karundevi
Department of Endocrinology, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai, Tamil Nadu, India.
Mol Cell Endocrinol. 2008 Mar 26;285(1-2):34-42. doi: 10.1016/j.mce.2008.01.020. Epub 2008 Feb 3.
The adverse effects of glucocorticoid deficiency on the expression of genes encoding Leydig cell surface receptors and the response to LH/prolactin/insulin to produce testosterone production are yet to be recognized. Following metyrapone-induced corticosterone deficiency, serum corticosterone, testosterone and insulin levels decrease, whereas serum prolactin exhibits a significant increase and serum LH remains unaltered. LH binding and LH receptor mRNA expression were not altered, but a significant decrease in PRL and insulin binding and in the mRNA expressions of their receptors were observed in corticosterone-deficient rats in vivo. Corticosterone deficiency significantly decreases the Leydig cellular basal as well as hormone-stimulated testosterone production in vitro. Simultaneous administration of corticosterone prevented its deficiency-induced changes in Leydig cells both in vivo and in vitro. Our results show that metyrapone-induced corticosterone deficiency impairs Leydig cell insulin and prolactin receptors, and their mRNA expression and the response of Leydig cells to LH/PRL/insulin on testosterone production.
糖皮质激素缺乏对编码睾丸间质细胞表面受体的基因表达以及对促黄体生成素/催乳素/胰岛素产生睾酮的反应的不利影响尚未得到认识。在甲吡酮诱导的皮质酮缺乏后，血清皮质酮、睾酮和胰岛素水平降低，而血清催乳素显著升高，血清促黄体生成素保持不变。促黄体生成素结合和促黄体生成素受体mRNA表达未改变，但在体内皮质酮缺乏的大鼠中观察到催乳素和胰岛素结合及其受体的mRNA表达显著降低。皮质酮缺乏在体外显著降低睾丸间质细胞基础以及激素刺激的睾酮产生。同时给予皮质酮可预防其在体内和体外缺乏诱导的睾丸间质细胞变化。我们的结果表明，甲吡酮诱导的皮质酮缺乏损害睾丸间质细胞胰岛素和催乳素受体及其mRNA表达以及睾丸间质细胞对促黄体生成素/催乳素/胰岛素产生睾酮的反应。
