Role of Follicle-Stimulating Hormone in Spermatogenesis.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanism-based reasoning, preclinical rodent models, and genetic case observations
PubMed 30619093 · doi:10.3389/fendo.2018.00763
What was done
Narrative review synthesizing mechanistic studies, rodent knockout models, human loss-of-function genetic mutations (in FSHB and FSHR), and transgenic mouse experiments evaluating the roles of follicle-stimulating hormone (FSH) and testosterone in spermatogenesis.
What was found
No quantitative data are reported in the abstract. Qualitatively, rodents complete spermatogenesis without FSH but have reduced sperm quantity, whereas humans with FSHB or FSHR loss-of-function mutations present with azoospermia or suppressed spermatogenesis. Spermatogenesis can proceed at minimal intratesticular testosterone levels, and constitutive FSH receptor activation rescued spermatogenesis and fertility in mice despite complete testosterone blockade.
Why it matters
Challenges the dogma that high intratesticular testosterone is strictly required for male fertility, providing a mechanistic basis for exploring high-dose FSH therapy in spermatogenic failure.
Limits
Narrative review with no systematic methodology or sample size reported. Primary interventional findings are restricted to transgenic animal models, and human observations rely on rare loss-of-function genetic mutations.
Cited by
- supports Sertoli cells support spermatogenesis and are regulated by follicle-stimulating hormone (FSH).