Armstrong D T, Papkoff H
Endocrinology. 1976 Oct;99(4):1144-51. doi: 10.1210/endo-99-4-1144.
The role of follicle-stimulating hormone (FSH) in the regulation of estrogen biosynthesis in vivo has been investigated in immature hypophysectomized rats, utilizing uterine weight and histologic responses, and ovarian estradiol-17beta concentrations as indicators of estrogen secretion. A highly purified FSH preparation produced only borderline increases in uterine weights and in ovarian estradiol-17beta contents when administered alone at 2.5 mug/day for 3 days. Testosterone or androstenedione (5 mg/day), when administered in the absence of FSH, produced typically androgenic stimulation of uteri, and did not increase ovarian estradiol-17beta concentrations. When administered concomitantly with FSH, the uterine weight-stimulating activity of these aromatizable androgens was substantially increased, accompanied by marked hypertrophy of the endometrial mucosal cells, and ovarian estradiol-17beta concentrations were increased 20- to 200-fold. The administration of the non-aromatizable androgen, 17beta-OH-5alpha-androstan-3-one (DHT) (5 mg/day, by itself produced uterine weight increases similar to those caused by testosterone alone; however, no evidence of increased estrogen secretion resulted from the combined treatment of DHT wtih FSH. A highly purified luteinizing hormone (LH) preparation was equally as effective as exogenous androstenedione in increasing ovarian concentrations of immunoreactive androgen (testosterone + DHT) but evoked none of the above signs of estrogen secretion unless administered together with FSH. The weights of ovaries were not affected by the administration of LH or of any of the androgens by themselves, but were approximately doubled by FSH alone. Ovarian weights were increased still further when FSH was administered concomitantly with LH, testosterone , or androstenedione, but not with DHT. It is concluded that FSH and LH regulate ovarian estrogen secretion in vivo by acting at biochemically distinct sites--LH stimulating the synthesis of C19-steroids, which are then converted to estradiol-17beta under specific stimulation by FSH.
利用子宫重量和组织学反应以及卵巢雌二醇 - 17β浓度作为雌激素分泌指标，在未成熟垂体切除大鼠中研究了促卵泡激素（FSH）在体内雌激素生物合成调节中的作用。当以2.5微克/天的剂量单独给药3天时，一种高度纯化的FSH制剂仅使子宫重量和卵巢雌二醇 - 17β含量略有增加。在没有FSH的情况下给予睾酮或雄烯二酮（5毫克/天），通常会对子宫产生雄激素刺激，并且不会增加卵巢雌二醇 - 17β浓度。当与FSH同时给药时，这些可芳香化雄激素的子宫重量刺激活性显著增加，伴随着子宫内膜粘膜细胞的明显肥大，并且卵巢雌二醇 - 17β浓度增加了20至200倍。给予不可芳香化雄激素17β - OH - 5α - 雄甾烷 - 3 - 酮（双氢睾酮，DHT）（5毫克/天），其本身导致的子宫重量增加与单独使用睾酮引起的相似；然而，DHT与FSH联合治疗没有导致雌激素分泌增加的证据。一种高度纯化的促黄体生成素（LH）制剂在增加卵巢中免疫反应性雄激素（睾酮+双氢睾酮）浓度方面与外源性雄烯二酮同样有效，但除非与FSH一起给药，否则不会引起上述任何雌激素分泌迹象。单独给予LH或任何一种雄激素对卵巢重量没有影响，但单独给予FSH可使卵巢重量增加约一倍。当FSH与LH、睾酮或雄烯二酮同时给药时，卵巢重量进一步增加，但与双氢睾酮同时给药时卵巢重量没有增加。结论是，FSH和LH通过作用于生化上不同的位点来调节体内卵巢雌激素分泌——LH刺激C19类固醇的合成，然后在FSH的特定刺激下将其转化为雌二醇 - 17β。
