Friend K E, Hartman M L, Pezzoli S S, Clasey J L, Thorner M O
Division of Endocrinology and Metabolism, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
J Clin Endocrinol Metab. 1996 Jun;81(6):2250-6. doi: 10.1210/jcem.81.6.8964860.
To determine if the mode of 17 beta-estradiol (E2) administration affects growth hormone (GH) concentrations, eight postmenopausal women were studied under the following conditions: (1) control (no E2), (2) oral E2 (Estrace, 1 mg every 12 h for 2 weeks) and (3) transdermal E2 (Estraderm patch, 0.1 mg, two patches changed daily for 2 weeks). Blood was collected every 5 min for 24 h and assayed for serum GH concentrations using a sensitive chemiluminescence assay. Serum E2 levels were comparable during both E2 treatment regimens when measured with a specific chemiluminescence assay. The 24-h integrated GH concentrations (IGHC, min . micrograms/L) increased in all eight subjects from (mean +/- SE) 494 +/- 102 during control to 860 +/- 111 (P < 0.05) and 832 +/- 149 (P < 0.05) during oral and transdermal E2, respectively. Both E2 treatments significantly increased GH pulse height, individual pulse area, incremental pulse amplitude, interpeak valley concentration, and interpeak valley nadir (as measured by Cluster algorithm) when compared with control. No significant differences were observed in the number of GH pulses per 24 h. Insulin-like growth factor-I (IGF-I, micrograms/L) concentrations decreased from 165 +/- 19 (control) to 109 +/- 11 (oral E2, P < 0.05) and 122 +/- 15 (transdermal E2, P < 0.05). No statistically significant differences in attributes of pulsatile GH release or IGF-I concentrations were observed between the oral and transdermal E2 treatments. We conclude that both oral and transdermal E2 treatment increase serum GH concentrations in postmenopausal women. This increase is manifested by larger GH pulses and higher basal (interpulse) GH levels, not by changes in pulse frequency. Both routes of E2 administration decrease serum IGF-I concentrations, which may attenuate IGF-I negative feedback on pituitary somatotrophs and hypothalamic somatostatin secretion, resulting in enhanced pulsatile GH release.
为确定17β-雌二醇（E2）的给药方式是否会影响生长激素（GH）浓度，对8名绝经后女性在以下条件下进行了研究：（1）对照（未用E2），（2）口服E2（Estrace，每12小时1 mg，共2周），以及（3）经皮E2（Estraderm贴片，0.1 mg，每天更换两片，共2周）。每5分钟采集一次血样，持续24小时，并使用灵敏的化学发光分析法检测血清GH浓度。使用特异性化学发光分析法测量时，两种E2治疗方案期间的血清E2水平相当。所有8名受试者的24小时整合GH浓度（IGHC，分钟·微克/升）从对照期间的（均值±标准误）494±102分别增至口服E2期间的860±111（P<0.05）和经皮E2期间的832±149（P<0.05）。与对照相比，两种E2治疗均显著增加了GH脉冲高度、单个脉冲面积、增量脉冲幅度、峰间谷浓度和峰间谷最低点（通过聚类算法测量）。每24小时的GH脉冲数量未观察到显著差异。胰岛素样生长因子-I（IGF-I，微克/升）浓度从165±19（对照）降至109±11（口服E2，P<0.05）和122±15（经皮E2，P<0.05）。口服和经皮E2治疗之间在脉冲式GH释放属性或IGF-I浓度方面未观察到统计学上的显著差异。我们得出结论，口服和经皮E2治疗均会增加绝经后女性的血清GH浓度。这种增加表现为更大的GH脉冲和更高的基础（脉冲间期）GH水平，而非脉冲频率的变化。两种E2给药途径均会降低血清IGF-I浓度，这可能会减弱IGF-I对垂体生长激素细胞和下丘脑生长抑素分泌的负反馈，从而导致脉冲式GH释放增强。
