ANDROGEN-STIMULATED PUBERTAL GROWTH - THE EFFECTS OF TESTOSTERONE AND DIHYDROTESTOSTERONE ON GROWTH-HORMONE AND INSULIN-LIKE GROWTH FACTOR-I IN THE TREATMENT OF SHORT STATURE AND DELAYED PUBERTY
ANDROGEN-STIMULATED PUBERTAL GROWTH - THE EFFECTS OF TESTOSTERONE AND DIHYDROTESTOSTERONE ON GROWTH-HORMONE AND INSULIN-LIKE GROWTH FACTOR-I IN THE TREATMENT OF SHORT STATURE AND DELAYED PUBERTY
复制标题
DOI：
10.1210/jc.76.4.996
复制
发表时间：
1993-04-01
影响因子：
5.8
通讯作者：
SMITH, ER
中科院分区：
文献类型：
--
作者：
KEENAN, BS;RICHARDS, GE;SMITH, ER
本研究的目的是探讨雄激素和雌激素机制在刺激男性青春期结构生长和血浆 GH 中的作用。为了解决这两种可能的机制，我们比较了两种雄激素在治疗体质性生长和青春期延迟中的效果：芳香化雄激素睾酮（T）和非芳香化雄激素二氢睾酮（DHT）。对 9 名处于 Tanner 1 期或 2 期的青少年男性在使用 T 庚酸酯（A 组）或 DHT 庚酸酯（B 组）治疗之前和治疗期间进行了研究。治疗 2.5 个月后，A 组的身高速度 (HV) 为 12.6 +/- 2.8 厘米/年 (n = 3)，B 组为 8.9 +/- 1.7 厘米/年 (n = 6)，均在青春期男性的峰值 HV 范围内。 A组GH积分浓度（ICGH）由3.12±0.90升高至13.67±6.0μg/L（P < 0.05），血浆胰岛素样生长因子-I（IGFI）由126.7±2.5升高至350.3±20.3μg/L（P < 0.01）；血浆 T 从 0.8 +/- 0.5 增加至 33.8 +/- 11.0 nmol/L (P < 0.001)，LH 对 LHRH 的反应从 27.6 +/- 10.7 降至 5.9 +/- 2.5 IU/L (P = NS)。 B组中，ICGH从4.32+/-0.61下降至2.39+/-0.42(P<0.025)，IGF-I从218.3+/-39.2下降至184.0+/-15.8(P=NS)。血浆 T 从 2.0 +/- 0.5 增加至 2.7 +/- 0.8 (P = NS)，LH 对 LHRH 的反应从 45.7 +/- 14.5 降至 10.7 +/- 5.8 (P < 0.05)。为了进一步评估 DHT 对血浆 GH 影响的机制，七名患有青春期男性乳房发育症的男性受试者接受了 DHT 庚酸酯治疗，并在 1 周和 3.5 个月时研究了他们的反应。 ICGH 随着积分 T 浓度的降低而降低（r = -0.77；P < 0.001），并且随着血浆雌二醇的降低而略有降低（r = -0.39；P < 0.2）。男性乳房发育症受试者的血浆 IGF-I 没有显示出显着变化。因此，男性青春期生长激素的增加似乎是由于雌激素依赖性机制。 DHT 对 GH 分泌的抑制作用可能是由于抑制雌二醇的产生或直接作用。 DHT 使 HV 加速进入青春期峰值范围，而血浆 GH 不增加，这表明 GH 的增加对于青春期生长突增来说并不是必需的。
The purpose of this study was to investigate the roles of androgenic and estrogenic mechanisms in the stimulation of structural growth and plasma GH in male puberty. To resolve these two possible mechanisms, we compared the effect of two androgens in the treatment of constitutional delay in growth and adolescence: an aromatizable androgen, testosterone (T), and a nonaromatizable androgen, dihydrotestosterone (DHT). Nine adolescent males, Tanner stage 1 or 2, were studied before and during treatment with T enanthate (group A) or DHT heptanoate (group B). After 2.5 months of treatment, the height velocity (HV) was 12.6 +/- 2.8 cm/yr (n = 3) in group A and 8.9 +/- 1.7 cm/yr (n = 6) in group B, both within the range of peak HV for pubertal males. In group A, the integrated concentration of GH (ICGH) increased from 3.12 +/- 0.90 to 13.67 +/- 6.0 mug/L (P < 0.05), and plasma insulin-like growth factor-I (IGFI) increased from 126.7 +/- 2.5 to 350.3 +/- 20.3 mug/L (P < 0.01); plasma T increased from 0.8 +/- 0.5 to 33.8 +/- 11.0 nmol/L (P < 0.001), and the LH response to LHRH decreased from 27.6 +/- 10.7 to 5.9 +/- 2.5 IU/L (P = NS). In group B, ICGH decreased from 4.32 +/- 0.61 to 2.39 +/- 0.42 (P < 0.025), and IGF-I decreased from 218.3 +/-39.2 to 184.0 +/- 15.8 (P = NS). Plasma T increased from 2.0 +/- 0.5 to 2.7 +/- 0.8 (P = NS), and the LH response to LHRH decreased from 45.7 +/- 14.5 to 10.7 +/- 5.8 (P < 0.05). To further evaluate the mechanism of the effect of DHT on plasma GH, seven male subjects with adolescent gynecomastia were treated with DHT heptanoate, and their responses were studied at 1 week and 3.5 months. ICGH decreased in conjunction with a decrease in the integrated T concentration (r = -0.77; P < 0.001) and to a slight degree with decreasing plasma estradiol (r = -0.39; P < 0.2). Plasma IGF-I did not show a significant change in the subjects with gynecomastia. Thus, the increase in GH at puberty in males appears to be due to an estrogen-dependent mechanism. The suppressive effect of DHT on GH secretion may be due to either suppression of estradiol production or a direct effect. Acceleration of HV into the peak pubertal range by DHT without an increase in plasma GH suggests that an increase in GH is not necessary for the pubertal growth spurt.