ArticleScientific reports2017
Involvement of gonadotropin-inhibitory hormone in pubertal disorders induced by thyroid status.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- The hippo pathway: a molecular bridge between environmental cues and pace of life.BMC ecology and evolution · 2025Review
- Treating Severe Primary Hypothyroidism: Turning Growth Failure Into Rapidly Progressive Puberty.Cureus · 2025Article
- Review
- Longitudinal Evaluation of Reproductive Endocrine Function in Men With ACTH-Dependent Cushing Syndrome.The Journal of clinical endocrinology and metabolism · 2025Article
- Unveiling the hidden: acquired pediatric hypothyroidism.Frontiers in endocrinology · 2025Review
- Mild Gestational Hypothyroidism in Mice Has Transient Developmental Effects and Long-Term Consequences on Neuroendocrine Systems.Thyroid : official journal of the American Thyroid Association · 2025Article
- The Thyroid Hormone Axis and Female Reproduction.International journal of molecular sciences · 2023Review
- RFRP-3 Influences Apoptosis and Steroidogenesis of Yak Cumulus Cells and Compromises Oocyte Meiotic Maturation and Subsequent Developmental Competence.International journal of molecular sciences · 2023Article
- Impact of stress on male fertility: role of gonadotropin inhibitory hormone.Frontiers in endocrinology · 2023Review
- Diabetes as a potential compounding factor in COVID-19-mediated male subfertility.Cell & bioscience · 2022Review
- Effects of Maternal Hypothyroidism on the Pubertal Development in Female Rat Offspring.Development & reproduction · 2021Article
- RF-amide related peptide-3 (RFRP-3): a novel neuroendocrine regulator of energy homeostasis, metabolism, and reproduction.Molecular biology reports · 2021Review
- Gonadotropin Inhibitory Hormone and Its Receptor: Potential Key to the Integration and Coordination of Metabolic Status and Reproduction.Frontiers in endocrinology · 2021Review
- Reproductive neuroendocrinology of mammalian gonadotropin-inhibitory hormone.Reproductive medicine and biology · 2019Review
- Editorial: Progress in Reproductive Neuroendocrinology in Vertebrates.Frontiers in endocrinology · 2019Article
- Molecular Mechanisms of Gonadotropin-Inhibitory Hormone (GnIH) Actions in Target Cells and Regulation of GnIH Expression.Frontiers in endocrinology · 2019Review
- The roles of RFamide-related peptides (RFRPs), mammalian gonadotropin-inhibitory hormone (GnIH) orthologues in female reproduction.Iranian journal of basic medical sciences · 2018Review
- Sexual precocity in a girl with early-onset Graves' disease.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2018Article
- How to Contribute to the Progress of Neuroendocrinology: Discovery of GnIH and Progress of GnIH Research.Frontiers in endocrinology · 2018Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid disorders cause abnormal puberty, indicating interactions between the hypothalamus-pituitary-thyroid (HPT) and hypothalamus-pituitary-gonadal (HPG) axes, which are important in pubertal development. The hypothalamic gonadotropin-inhibitory hormone (GnIH) was shown to be decreased in the early prepubertal stage, suggesting the role of GnIH on pubertal onset. Here, we investigated whether thyroid dysfunction affects pubertal onset in female mice via GnIH regulation. Hypothyroidism showed delayed pubertal onset with increased GnIH expression and reduced pituitary-gonadal activity. Remarkably, knockout of GnIH prevented the effect of hypothyroidism to delay the pubertal onset, resulting in indistinguishable pubertal timing in GnIH-knockout female mice between control and hypothyroidism-induced group, indicating that increased GnIH expression induced by hypothyroidism may lead to delayed puberty. In contrast, hyperthyroidism led to a decrease in GnIH expression, however pubertal onset was normal, implying further reduction of the inhibitory GnIH had little effect on the phenotypical change. Critically, thyroid hormone suppressed GnIH expression in hypothalamic explants and GnIH neurons expressed thyroid hormone receptors to convey the thyroid status. Moreover, the thyroid status highly regulated the chromatin modifications of GnIH promoter, H3acetylation and H3K9tri-methylation. These findings indicate a novel function of GnIH to mediate HPT-HPG interactions that contribute to proper pubertal development.
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