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Vertebrate gonadal function is regulated by pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). These hormones are considered to be regulated by hypothalamic factor(s). Since the discovery of gonadotropin-releasing hormone (GnRH) in mammals, which stimulates the secretion of both FSH and LH, GnRH had been believed to be the sole gonadotropin-releasing hormone in vertebrates for more than 5 decades. However, recent studies have identified an alternative primary regulator of FSH in teleosts, leading to the hypothesis that FSH and LH are regulated by different factors in teleosts (dual GnRH model). This contrasts with the situation in mammals, where a single GnRH regulates both hormones (solo GnRH model). Importantly, although underlying mechanisms likely differ, both teleosts and mammals reproduce efficiently and have convergently evolved similar phenomena, including steroid feedback regulation. In this review, by comparing these taxa, we summarize mechanistic differences and propose an evolutionary scenario based on current experimental evidence.
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http://dx.doi.org/10.1002/bies.70066 | DOI Listing |
Bioessays
September 2025
Atmosphere and Ocean Research Institute, The University of Tokyo, Kashiwa, Chiba, Japan.
Vertebrate gonadal function is regulated by pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). These hormones are considered to be regulated by hypothalamic factor(s). Since the discovery of gonadotropin-releasing hormone (GnRH) in mammals, which stimulates the secretion of both FSH and LH, GnRH had been believed to be the sole gonadotropin-releasing hormone in vertebrates for more than 5 decades.
View Article and Find Full Text PDFInt J Gynaecol Obstet
September 2025
Department of Gynecology and Obstetrics, Justus Liebig University Giessen, Giessen, Germany.
Even though uterine fibroids are a widespread condition, the range of approved medical treatment options remains limited. In fact, only a few drugs are officially approved for the therapy of fibroids. In both the USA and the European Medicines Agency region, selected gonadotropin-releasing hormone (GnRH) antagonists have been approved for this indication.
View Article and Find Full Text PDFIntroduction: Congenital Hypogonadotropic Hypogonadism (CHH) arises from defects in the synthesis, secretion, or action of gonadotropin-releasing hormone (GnRH), resulting in incomplete or absent pubertal development and various non-reproductive features. CHH is genetically heterogeneous, with over 50 genes implicated in its pathogenesis. This study aimed to elucidate the genetic variants of CHH in a cohort of patients from a single-center endocrinology unit.
View Article and Find Full Text PDFStem Cell Rev Rep
September 2025
Stem Cells and Metabolism Research Program (STEMM), Research Programs Unit, Faculty of Medicine, University of Helsinki, Helsinki, 00014, Finland.
Mutations in Delta Like Non-Canonical Notch Ligand 1 (DLK1), a paternally expressed imprinted gene, underlie central precocious puberty (CPP), yet the mechanism remains unclear. To test the hypothesis that DLK1 plays a role in gonadotropin releasing hormone (GnRH) neuron ontogeny, 75 base pairs were deleted in both alleles of DLK1 exon 3 with CRISPR-Cas9 in human pluripotent stem cells (hPSCs). This line, exhibiting More than 80% loss of DLK1 protein, was differentiated into GnRH neurons by dual SMAD inhibition (dSMADi), FGF8 treatment and Notch inhibition, as previously described, however, it did not exhibit accelerated GNRH1 expression.
View Article and Find Full Text PDFAnn Afr Med
September 2025
Department of Pathology, Dr. Lal Path Labs, New Delhi, India.
Luteinizing hormone-releasing hormone agonists, used in advanced prostate cancer, can cause an initial testosterone surge and may inadequately suppress follicle-stimulating hormone, potentially promoting tumor growth. Injectable gonadotropin-releasing hormone (GnRH) antagonists avoid this surge but have drawbacks like injection-site reactions and monthly dosing. Relugolix, an oral GnRH antagonist, offers rapid testosterone suppression without flare and reduced cardiovascular risks.
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