Messinis I E, Lolis D, Zikopoulos K, Milingos S, Kollios G, Seferiadis K, Templeton A A
Department of Obstetrics and Gynaecology, University of Ioannina, Greece.
Clin Endocrinol (Oxf). 1996 Feb;44(2):169-75. doi: 10.1046/j.1365-2265.1996.589411.x.
Although there is much in-vivo evidence for the existence of a gonadotrophin surge attenuating factor (GnSAF), its source and identity remain unknown. We have studied the control of GnSAF production by FSH and hCG during the luteal phase of the cycle.
Normally cycling women were investigated in three cycle. Starting on day 5 after the midcycle LH peak, the women received i.m. injections of placebo (1st cycle control), hCG at a dose of 750 IU per day (2nd cycle) and FSH at a dose of 225 IU per day (3rd cycle) for five consecutive days. The response of LH to a single i.v. dose of 10 microg GnRH (GnSAF bioactivity) was investigated several times during the experimental period.
Six normally ovulating women with long-standing unexplained infertility were studied. The women were used as their own controls during the cycle treated with placebo.
Pituitary response to GnRH was calculated as the net increase in LH at 30 minutes (deltaLH) above the basal value.
Serum concentrations of FSH and hCG increased significantly during the second and 3rd cycles respectively. Compared with the control cycles, deltaLH was significantly attenuated as early as 12 hours from the onset of FSH injections. In contrast, basal concentrations of oestradiol (E2) and immunoreactive inhibin started to increase 48 hours after the first injection of FSH, while progesterone values remained similar to those in the controls. During treatment with hCG, no attenuation was seen in deltaLH values, while those of E2, progesterone and inhibin showed a significant increase.
These results demonstrate that during the luteal phase of the human menstrual cycle, FSH, but not LH, stimulates the production of gonadotrophin surge attenuating factor. It is suggested that the source of gonadotrophin surge attenuating factor at that stage of the cycle is a cohort of small follicles rather than the corpus luteum.
尽管有大量体内证据表明存在促性腺激素激增衰减因子（GnSAF），但其来源和特性仍不清楚。我们研究了在月经周期黄体期，促卵泡激素（FSH）和人绒毛膜促性腺激素（hCG）对GnSAF产生的调控作用。
对月经周期正常的女性进行三个周期的研究。从中周期促黄体生成素（LH）峰后的第5天开始，这些女性连续5天接受肌肉注射安慰剂（第1周期对照）、每天750国际单位的hCG（第2周期）和每天225国际单位的FSH（第3周期）。在实验期间多次研究LH对单次静脉注射10微克促性腺激素释放激素（GnRH）（GnSAF生物活性）的反应。
研究了6名长期不明原因不孕但排卵正常的女性。在接受安慰剂治疗的周期中，这些女性以自身作为对照。
垂体对GnRH的反应以30分钟时LH相对于基础值的净增加量（ΔLH）来计算。
FSH和hCG的血清浓度在第2和第3周期分别显著升高。与对照周期相比，早在注射FSH开始后12小时，ΔLH就显著降低。相比之下，雌二醇（E2）和免疫反应性抑制素的基础浓度在首次注射FSH后48小时开始升高，而孕酮值与对照相似。在hCG治疗期间，ΔLH值未见降低，而E2、孕酮和抑制素的值显著升高。
这些结果表明，在人类月经周期的黄体期，是FSH而非LH刺激了促性腺激素激增衰减因子的产生。提示在月经周期该阶段促性腺激素激增衰减因子的来源是一群小卵泡而非黄体。
