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      Real-world evidence analysis of the follicle-stimulating hormone use in male idiopathic infertility

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      Best Practice & Research Clinical Obstetrics & Gynaecology
      Elsevier BV

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          Real-World Evidence - What Is It and What Can It Tell Us?

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            Genetics of male infertility

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              Follicle stimulating hormone is required for ovarian follicle maturation but not male fertility.

              Follicle stimulating hormone (FSH) is a member of the glycoprotein hormone family that includes luteinzing hormone (LH), thyroid stimulating hormone, and chorionic gonadotropin. These heterodimeric hormones share a common alpha subunit and differ in their hormone-specific beta subunit. The biological activity is conferred only by the heterodimers. FSH and LH are synthesized in the same cells of the pituitary, the gonadotrophs. FSH receptors are localized to Sertoli cells of the testes and granulosa cells of the ovary. Minimal data has been accumulated so far involving human mutations in the FSH beta, LH beta, or the gonadotropin receptor genes. There are no known mouse strains with mutations in the FSH beta gene. To generate animal models for human diseases involving the gonadotropin signal transduction pathway, we produced mice deficient in the FSH beta subunit and therefore in FSH using ES cell technology. FSH-deficient females are infertile due to a block in folliculogenesis prior to antral follicle formation. Although FSH was predicted to be necessary for spermatogenesis and Sertoli cell growth in males, FSH-deficient males are fertile despite having small testes. Our findings have important implications for male contraceptive development in humans.
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                Journal
                Best Practice & Research Clinical Obstetrics & Gynaecology
                Best Practice & Research Clinical Obstetrics & Gynaecology
                Elsevier BV
                15216934
                December 2022
                December 2022
                : 85
                : 121-133
                Article
                10.1016/j.bpobgyn.2022.04.004
                bdc9de9e-a32a-48cb-af0c-2113277cf858
                © 2022

                https://www.elsevier.com/tdm/userlicense/1.0/

                https://doi.org/10.15223/policy-017

                https://doi.org/10.15223/policy-037

                https://doi.org/10.15223/policy-012

                https://doi.org/10.15223/policy-029

                https://doi.org/10.15223/policy-004

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