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The Roles of Luteinizing Hormone, Follicle-Stimulating Hormone and Testosterone in Spermatogenesis and Folliculogenesis Revisited

1
Institute of Reproductive and Developmental Biology, Department of Metabolism, Digestion and Reproduction, Imperial College London, Hammersmith Hospital Campus, London W12 0NN, UK
2
Institute of Biomedicine, University of Turku, 20520 Turku, Finland
3
Unité de Génétique Moléculaire des Maladies Métaboliques et de la Reproduction, APHP Hôpitaux Universitaires Paris-Saclay, Hôpital Bicêtre, Faculté de Médecine Paris Saclay, 94275 Le Kremlin-Bicêtre, France
4
Hôpital Paul Brousse, Université Paris Saclay, UMR-S 1193, INSERM, 94800 Villejuif, France
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Marco Falasca
Int. J. Mol. Sci. 2021, 22(23), 12735; https://doi.org/10.3390/ijms222312735
Received: 8 October 2021 / Revised: 11 November 2021 / Accepted: 12 November 2021 / Published: 25 November 2021
Spermatogenesis and folliculogenesis involve cell–cell interactions and gene expression orchestrated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). FSH regulates the proliferation and maturation of germ cells independently and in combination with LH. In humans, the requirement for high intratesticular testosterone (T) concentration in spermatogenesis remains both a dogma and an enigma, as it greatly exceeds the requirement for androgen receptor (AR) activation. Several data have challenged this dogma. Here we report our findings on a man with mutant LH beta subunit (LHβ) that markedly reduced T production to 1–2% of normal., but despite this minimal LH stimulation, T production by scarce mature Leydig cells was sufficient to initiate and maintain complete spermatogenesis. Also, in the LH receptor (LHR) knockout (LuRKO) mice, low-dose T supplementation was able to maintain spermatogenesis. In addition, in antiandrogen-treated LuRKO mice, devoid of T action, the transgenic expression of a constitutively activating follicle stimulating hormone receptor (FSHR) mutant was able to rescue spermatogenesis and fertility. Based on rodent models, it is believed that gonadotropin-dependent follicular growth begins at the antral stage, but models of FSHR inactivation in women contradict this claim. The complete loss of FSHR function results in the complete early blockage of folliculogenesis at the primary stage, with a high density of follicles of the prepubertal type. These results should prompt the reassessment of the role of gonadotropins in spermatogenesis, folliculogenesis and therapeutic applications in human hypogonadism and infertility. View Full-Text
Keywords: spermatogenesis; folliculogenesis; FSH; LH; testosterone; mutation; intratesticular testosterone; azoospermia; Sertoli cell; Leydig cell; minipuberty; knock-out mice spermatogenesis; folliculogenesis; FSH; LH; testosterone; mutation; intratesticular testosterone; azoospermia; Sertoli cell; Leydig cell; minipuberty; knock-out mice
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MDPI and ACS Style

Oduwole, O.O.; Huhtaniemi, I.T.; Misrahi, M. The Roles of Luteinizing Hormone, Follicle-Stimulating Hormone and Testosterone in Spermatogenesis and Folliculogenesis Revisited. Int. J. Mol. Sci. 2021, 22, 12735. https://doi.org/10.3390/ijms222312735

AMA Style

Oduwole OO, Huhtaniemi IT, Misrahi M. The Roles of Luteinizing Hormone, Follicle-Stimulating Hormone and Testosterone in Spermatogenesis and Folliculogenesis Revisited. International Journal of Molecular Sciences. 2021; 22(23):12735. https://doi.org/10.3390/ijms222312735

Chicago/Turabian Style

Oduwole, Olayiwola O., Ilpo T. Huhtaniemi, and Micheline Misrahi. 2021. "The Roles of Luteinizing Hormone, Follicle-Stimulating Hormone and Testosterone in Spermatogenesis and Folliculogenesis Revisited" International Journal of Molecular Sciences 22, no. 23: 12735. https://doi.org/10.3390/ijms222312735

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