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正常男性及特发性低促性腺激素性性腺功能减退男性在促甲状腺激素释放激素刺激后的垂体糖蛋白激素α亚基分泌情况。

Pituitary glycoprotein hormone alpha-subunit secretion after thyrotropin-releasing hormone stimulation in normal men and men with idiopathic hypogonadotropic hypogonadism.

作者信息

Winters S J, Troen P

机构信息

Department of Medicine, Montefiore Hospital, Pittsburgh, Pennsylvania 15213.

出版信息

J Clin Endocrinol Metab. 1990 Feb;70(2):544-7. doi: 10.1210/jcem-70-2-544.

Abstract

Although TRH stimulates the release of uncombined alpha-subunit into the circulation in patients with primary hypothyroidism, it is not clear whether alpha-subunit is released from the thyrotrophs in euthyroid subjects. We hypothesized that spontaneous fluctuations in circulating alpha-subunit released from gonadotrophs by GnRH in normal adults could obscure the detection of small changes in alpha-subunit after TRH administration. We, therefore, examined alpha-subunit responses to TRH in five euthyroid men with idiopathic hypogonadotropic hypogonadism (IHH), who produce little or no GnRH, five normal men, and four postmenopausal women. Mean (+/- SEM) basal serum alpha-subunit levels were significantly (P less than 0.05) less in men with IHH (0.26 +/- 0.07 microgram/L) than in the normal men (0.80 +/- 0.20 microgram/L) or postmenopausal women (3.54 +/- 0.60 microgram/L). alpha-Subunit levels rose after TRH administration in all men with IHH to a peak level of 0.86 +/- 0.25 ng/ml; TSH levels also increased from 1.9 +/- 0.4 to 13.0 +/- 5.6 mU/L. The increment in TSH and alpha-subunit levels was highly positively correlated (r = 0.96). alpha-Subunit levels also increased 2-fold in normal men given TRH, whereas alpha-subunit levels in postmenopausal women were unchanged. We conclude that thyrotrophs release alpha-subunit into the circulation in normal men and euthyroid men with IHH. Thus, both thyrotrophs and gonadotrophs appear to contribute to circulating alpha-subunit in men with IHH; however, most of the uncombined alpha-subunit in normal men appears to be from gonadotrophs.

摘要

虽然促甲状腺激素释放激素(TRH)可刺激原发性甲状腺功能减退患者将未结合的α亚基释放到循环中,但尚不清楚甲状腺功能正常的受试者的促甲状腺细胞是否会释放α亚基。我们推测,正常成年人中促性腺激素释放激素(GnRH)刺激促性腺细胞释放的循环α亚基的自发波动,可能会掩盖TRH给药后α亚基微小变化的检测。因此,我们检测了5名患有特发性低促性腺激素性性腺功能减退(IHH)、几乎不产生或不产生GnRH的甲状腺功能正常男性、5名正常男性和4名绝经后女性对TRH的α亚基反应。患有IHH的男性的平均(±标准误)基础血清α亚基水平(0.26±0.07微克/升)显著低于正常男性(0.80±0.20微克/升)或绝经后女性(3.54±0.60微克/升)(P<0.05)。所有患有IHH的男性在给予TRH后α亚基水平升高至峰值水平0.86±0.25纳克/毫升;促甲状腺激素(TSH)水平也从1.9±0.4升高至13.0±5.6毫国际单位/升。TSH和α亚基水平的增量高度正相关(r = 0.96)。给予TRH的正常男性的α亚基水平也增加了2倍,而绝经后女性的α亚基水平未改变。我们得出结论,在正常男性和患有IHH的甲状腺功能正常男性中,促甲状腺细胞会将α亚基释放到循环中。因此,在患有IHH的男性中,促甲状腺细胞和促性腺细胞似乎都对循环中的α亚基有贡献;然而,正常男性中大多数未结合的α亚基似乎来自促性腺细胞。

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