Simultaneous increases of leptin and gonadotropin-releasing hormone following exogenous estrogen administration in women with normally menstrual cycle

Simultaneous increases of leptin and gonadotropin-releasing hormone following exogenous estrogen administration in women with normally menstrual cycle
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DOI:
10.1507/endocrj.52.449
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发表时间:
2005-08-01
期刊:
影响因子:
2
通讯作者:
Fujii, S
Fujii, S
中科院分区:
医学4区
文献类型:
--
作者:
Lin, KC;Sagawa, N;Fujii, S

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本研究旨在探讨外源性雌激素对正常月经周期妇女血清瘦素和促性腺激素释放激素(GnRH)水平的影响。18例妇女于月经周期第5天08:00静脉注射结合雌激素20 mg(倍美力组),另18例妇女静脉注射生理盐水20 mL(对照组)。分别于注射后0、4、8、24、28、32、48、56、72和96 h空腹采血,测定血清瘦素、促性腺激素释放激素(GnRH)、雌酮(E-1)、雌二醇(E-2)、LH和FSH。注射倍美力后,E-1和E-2的平均血浆水平从4小时开始显著升高,并显著持续升高至72小时。在注射后28、32和48小时观察到瘦素和GnRH水平同时显著增加,而对照组保持不变。平均LH和FSH水平最初受到抑制,然后在倍美力给药后56和72小时显著升高。瘦素可能通过传递代谢信号影响下丘脑GnRH的释放,参与雌激素正反馈机制的调节,但其是否参与负反馈机制的调节尚不清楚。
The aim of this study was to investigate whether administration of exogenous estrogen affects the changes of leptin and GnRH levels in women with normal menstrual cycle. A total of 18 women received a bolus intravenous injection of 20 mg conjugated estrogen (premarin group) at 0800 during the fifth day of menstrual cycle, while another 18 women were administered 20 mL of normal saline as the control group. Fasting blood samples were collected at 0, 4, 8, 24, 28, 32, 48, 56, 72 and 96 hours after injection for analyses of leptin, GnRH, estrone (E-1), estradiol (E-2), LH and FSH. Both the mean plasma levels of E-1 and E-2 were significantly increased from 4 hours and significantly sustained elevated levels up to 72 hours after injection of premarin. Simultaneous significant increases of leptin and GnRH levels were observed at 28, 32 and 48 hours after injection, while the controls remained constant. The mean LH and FSH levels were initially suppressed and then significantly increased at 56 and 72 hours after premarin administration. Leptin appears to be involved in the regulation of positive feedback mechanism of estrogen by conveyance of metabolic signal to affect the release of GnRH in hypothalamus, while its participation in the modulation of negative feedback remains unknown.