Production of testosterone is under tight control by human chorion gonadotropin (hCG) during fetal life and luteinizing hormone (LH) in adulthood. Several animal and human studies have linked vitamin D status with sex steroid production although it is not clear whether there exist a direct or indirect involvement in androgen production. Few studies have investigated this crosslink in young healthy men and putative direct or synergistic effect of activated vitamin D (1,25(OH)2D3) and LH/hCG on sex steroid production in vitro. Here, we present cross-sectional data from 300 young men and 41 hCG-stimulated men with impaired Leydig cell function combined with data from an ex vivo culture of human testicular tissue exposed to 1,25(OH)2D3 alone or in combination with hCG. Serum 25-OHD was positively associated with SHBG (β:0.002; p = 0.023) and testosterone/estradiol-ratio (β:0.001; p = 0.039), and inversely associated with free testosterone (%) (free testosterone/total testosterone) (β:-0.002; p = 0.016) in young men. Vitamin D deficient men had higher total and free estradiol concentrations than men with higher vitamin D status (19% and 18%, respectively; p < 0.01). Interestingly, men with impaired Leydig cell function and vitamin D deficiency had a significantly lower hCG-mediated increase in total and free testosterone compared with vitamin D sufficient men (p < 0.05). Accordingly, testicular tissue exposed to 100 nM 1,25(OH)2D3 had a 15% higher testosterone release into the media compared with vehicle treated specimens (p = 0.030). In conclusion, vitamin D deficiency is associated with lower testosterone/estradiol ratio in young men and lower Leydig cell sensitivity after hCG-stimulation in men with impaired gonadal function. The significant effect of 1,25(OH)2D3 on testosterone production in a human testis model supports that the stimulatory effect at least in part may be direct. Larger placebo-controlled studies are needed to determine whether vitamin D supplementation can influence testosterone production.

中文翻译：

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Leydig细胞功能正常或受损的男性的维生素D和性类固醇生成。

胎儿生命期间人绒毛膜促性腺激素（hCG）和成年期的促黄体生成激素（LH）严格控制着睾丸激素的产生。尽管尚不清楚是否直接或间接参与雄激素的产生，但一些动物和人体研究已将维生素D的状态与性类固醇的产生联系起来。很少有研究调查年轻健康男性中的这种交联以及活化的维生素D（1,25（OH）2D3）和LH / hCG对性类固醇体外产生的直接或协同作用。在这里，我们提供了300例Leydig细胞功能受损的年轻男性和41个hCG刺激的男性的横断面数据，以及单独或与hCG组合暴露于1,25（OH）2D3的人睾丸组织离体培养的数据。血清25-OHD与SHBG正相关（β：0.002; p = 0。023）和睾丸激素/雌二醇比率（β：0.001; p = 0.039），与年轻男性的游离睾丸激素（％）（游离睾丸激素/总睾丸激素）（β：-0.002; p = 0.016）成反比。维生素D缺乏症的男性比维生素D状况较高的男性具有更高的总雌二醇和游离雌二醇浓度（分别为19％和18％； p <0.01）。有趣的是，与足够摄取维生素D的男性相比，患有Leydig细胞功能受损和缺乏维生素D的男性的hCG介导的总睾丸激素和游离睾丸激素的增加显着较低（p <0.05）。因此，与媒介物处理过的标本相比，暴露于100 nM 1,25（OH）2D3的睾丸组织具有更高的15％睾丸激素向培养基中的释放（p = 0.030）。结论，维生素D缺乏症与性腺功能受损的男性hCG刺激后年轻男性的睾丸激素/雌二醇比值降低和Leydig细胞敏感性降低有关。1,25（OH）2D3对人睾丸模型中睾丸激素产生的显著作用表明，刺激作用至少部分是直接的。需要更大的安慰剂对照研究来确定补充维生素D是否会影响睾丸激素的产生。