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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The low gonadotropin-independent constitutive production of testicular testosterone is sufficient to maintain spermatogenesis
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The low gonadotropin-independent constitutive production of testicular testosterone is sufficient to maintain spermatogenesis

机译:低促性腺激素非依赖性的睾丸睾丸激素组成性生产足以维持精子发生

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Spermatogenesis is thought to critically depend on the high intra-testicular testosterone (T) levels induced by gonadotropic hormones. Strategies for hormonal male contraception are based on disruption of this regulatory mechanism through blockage of gonadotropin secretion. Although exogenous T or T plus progestin treatments efficiently block gonadotropin secretion and suppress testicular T production, only ≈ 60% of treated Caucasian men reach contraceptive azoospermia. We now report that in luteinizing hormone receptor knockout mice, qualitatively full spermatogenesis, up to elongated spermatids of late stages 13-16, is achieved at the age of 12 months, despite absent luteinizing hormone action and very low intratesticular T (2% of control level). However, postmeiotic spermiogenesis was blocked by the antiandrogen flutamide, indicating a crucial role of the residual low testicular T level in this process. The persistent follicle-stimulating hormone action in luteinizing hormone receptor knockout mice apparently stimulates spermatogenesis up to postmeiotic round spermatids, as observed in gonadotropin-deficient rodent models on follicle-stimulating hormone supplementation. The finding that spermatogenesis is possible without a luteinizing hormone-stimulated high level of intratesticular T contradicts the current dogma. Extrapolated to humans, it may indicate that only total abolition of testicular androgen action will result in consistent azoospermia, which is necessary for effective male contraception.
机译:精子发生被认为主要取决于促性腺激素诱导的睾丸内睾丸激素水平高。男性荷尔蒙避孕的策略是通过阻断促性腺激素分泌来破坏这种调节机制。尽管外源性T或T加孕激素治疗可以有效地阻断促性腺激素的分泌并抑制睾丸T的产生,但仅约60%的经治疗的白种人男性会达到避孕无精症。我们现在报道在黄体激素受体敲除小鼠中,尽管缺乏黄体激素作用和极低的睾丸内T(在对照组中的2%),但在12个月时达到了定性的完全生精作用,直至13-16后期的细长精子细胞。水平)。然而,减数分裂后的精子发生被抗雄激素氟他胺所阻止,表明残留的低睾丸T水平在该过程中起着至关重要的作用。在促黄体素缺乏的啮齿类动物补充卵泡刺激素的过程中观察到,在促黄体激素受体敲除小鼠中持续的卵泡刺激激素作用显然会刺激直至减数分裂后的圆形精子细胞的精子发生。没有黄体生成激素刺激的睾丸内T水平升高,精子发生是可能的发现与当前的教条相矛盾。推断到人类,这可能表明仅完全取消睾丸雄激素作用将导致一致的无精症,这对于有效的男性避孕是必要的。

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