Nieschlag E, Kley H K
Horm Metab Res. 1975 Jul;7(4):326-30. doi: 10.1055/s-0028-1093723.
In order to assess possible adrenal-testicular interactions in vivo, adrenal and testicular plasma androgens (testosterone, delta4-androstenedione, dehydroepiandrosterone and dehydroepiandrosterone sulfate) were measured by specific radioimmunoassays before and after stimulation with HCG in men with normal, dexamethasone suppressed and impaired adrenal function. It was found that men with Addison's disease, in whom circulating dehydroepiandrosterone sulfate levels amounted to 1/10 of normal values, had a decreased response of testosterone to HCG. Simultaneously, the Addison patients and the men under dexamethasone had only an increase of delta4-androstenedione but not of dehydroepiandrosterone, while normal men showed an almost equal increase in both precursors under HCG. The results are interpreted as demonstrating that the delta5-pathway in the testis becomes less important under adrenal suppression and in Addison's disease due to a lack of substrate (possibly dehydroepiandrosterone sulfate) from the adrenals.
为了评估体内肾上腺与睾丸之间可能存在的相互作用,我们采用特异性放射免疫分析法,对肾上腺功能正常、地塞米松抑制及肾上腺功能受损的男性,在人绒毛膜促性腺激素(HCG)刺激前后测定其肾上腺和睾丸血浆雄激素(睾酮、Δ4-雄烯二酮、脱氢表雄酮及硫酸脱氢表雄酮)水平。结果发现,艾迪生病患者循环硫酸脱氢表雄酮水平仅为正常值的1/10,其睾酮对HCG的反应降低。同时,艾迪生病患者及接受地塞米松治疗的男性,仅Δ4-雄烯二酮增加,而脱氢表雄酮未增加,而正常男性在HCG刺激下两种前体物质增加几乎相等。这些结果被解释为表明,由于肾上腺缺乏底物(可能是硫酸脱氢表雄酮),在肾上腺抑制及艾迪生病状态下,睾丸中的Δ5途径重要性降低。