Ewing L L, Wing T Y, Cochran R C, Kromann N, Zirkin B R
Endocrinology. 1983 May;112(5):1763-9. doi: 10.1210/endo-112-5-1763.
Hypophysectomy or sc implantation of testosterone-estradiol 17 beta (T-E) filled polydimethylsiloxane capsules for 5 days caused a dramatic reduction in testosterone secretion when testes subsequently were perfused in vitro. The diminution in testosterone-secreting capacity of testes from T-E treated rats was coupled closely with reductions in the membrane surface areas of Leydig cell cytoplasmic organelles, particularly those of the smooth endoplasmic reticulum. Simultaneous treatment of T-E implanted rats with LH (12 micrograms/day), but not with FSH, PRL, TSH, or GH, maintained both the Leydig-cell cytoplasmic membranes and the capacity of testes to secrete testosterone in vitro. Testosterone secretion by testes from hypophysectomized rats treated simultaneously with T-E plus LH was identical to that in control rats. Therefore, T-E did not inhibit directly the Leydig cell steroidogenic apparatus. Taken together these results suggest that one of the trophic effects of LH in the Leydig cell is to maintained the integrity of smooth endoplasmic reticulum and enzymes responsible for the conversion of pregnenolone to testosterone.
垂体切除或植入填充睾酮 - 雌二醇17β(T - E)的聚二甲基硅氧烷胶囊5天,会导致随后在体外灌注睾丸时睾酮分泌急剧减少。T - E处理的大鼠睾丸分泌睾酮能力的降低与莱迪希细胞胞质细胞器膜表面积的减少密切相关,尤其是滑面内质网的膜表面积。用LH(12微克/天)同时处理植入T - E的大鼠,但不用FSH、PRL、TSH或GH,可维持莱迪希细胞胞质膜以及睾丸在体外分泌睾酮的能力。同时用T - E加LH处理的垂体切除大鼠的睾丸分泌的睾酮与对照大鼠相同。因此,T - E并未直接抑制莱迪希细胞的类固醇生成装置。综合这些结果表明,LH在莱迪希细胞中的一种营养作用是维持滑面内质网和负责将孕烯醇酮转化为睾酮的酶的完整性。