Exogenous kisspeptin administration as a probe of GnRH neuronal function in patients with idiopathic hypogonadotropic hypogonadism
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CONTEXT: Idiopathic hypogonadotropic hypogonadism (IHH) results from defective synthesis, secretion, or action of GnRH. Kisspeptin is a potent stimulus for GnRH secretion. OBJECTIVE: We probed the functional capacity of the GnRH neuronal network in patients with IHH. PARTICIPANTS: Eleven subjects with congenital IHH (9 men and 2 women) and one male subject who underwent reversal of IHH were studied. Six of the twelve subjects had an identified genetic cause of their IHH: KAL1 (n = 1), FGFR1 (n = 3), PROKR2 (n = 1), GNRHR (n = 1). INTERVENTION: Subjects underwent q10 min blood sampling to measure GnRH-induced LH secretion at baseline and in response to intravenous boluses of kisspeptin (0.24 nmol/kg) and GnRH (75 ng/kg) both pre- and post-six days of treatment with exogenous GnRH (25 ng/kg sc every 2 h). RESULTS: All subjects with abiding IHH failed to demonstrate a GnRH-induced LH response to exogenous kisspeptin. In contrast, the subject who achieved reversal of his hypogonadotropism demonstrated a robust response to kisspeptin. CONCLUSIONS: The functional capacity of the GnRH neuronal network in IHH patients is impaired, as evidenced by their inability to respond to the same dose of kisspeptin that effects a robust GnRH-induced LH response in healthy men and luteal-phase women. This impairment is observed across a range of genotypes, suggesting that it reflects a fundamental property of GnRH neuronal networks that have not been properly engaged during pubertal development. In contrast, a patient who had experienced reversal of his hypogonadotropism responded to exogenous kisspeptin.
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In patients with idiopathic hypogonadotropic hypogonadism (IHH), the same weight-based dose of IV kisspeptin failed to stimulate an LH response.
“This stands in contrast to patients with idiopathic hypogonadotropic hypogonadism (IHH), in which the same weight-based dose of IV kisspeptin failed to stimulate an LH response (37).”
From Kisspeptin Overcomes GnRH Neuronal Suppression Secondary to Hyperprolactinemia in Humans (2022) · cites this paper as [37]
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Lippincott, M. F., Nguyen, K., Delaney, A., Chan, Y.-M., & Seminara, S. B. (2018) · Journal of the Endocrine Society · doi:10.1210/js.2018-00183 · Cited by 4 · see citing works
Kisspeptins Regulating Fertility: Potential Future Therapeutic Approach in Infertility Treatment
Kotanidou, S., Nikolettos, N., Kritsotaki, N., Tsikouras, P. N., Tiptiri-Kourpeti, A., & Nikolettos, K. (2025) · Journal of Clinical Medicine · doi:10.3390/jcm14103284 · Cited by 4 · see citing works
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Stoynev, N., & Kumanov, P. (2025) · Annales d Endocrinologie · doi:10.1016/j.ando.2025.101793 · Cited by 4 · see citing works
Lv, W., Jin, S., Wang, N., Cao, D., Jin, X., & Zhang, Y. (2021) · Comparative Biochemistry and Physiology Part D Genomics and Proteomics · doi:10.1016/j.cbd.2021.100831 · Cited by 3 · see citing works
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Gou, W., Xue, C., Zeng, F., Zhu, C., & Yang, B. (2025) · Renal Failure · doi:10.1080/0886022x.2025.2565406 · Cited by 1 · see citing works
Reversal of Congenital Hypogonadotropic Hypogonadism
Dwyer, A. A., & Stamou, M. I. (2025) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgaf610 · Cited by 1 · see citing works
Dynamic modulation of LH secretion by continuous kisspeptin infusion in healthy men
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Camera, M., Russo, I., Zamboni, V., Ammoni, A., Rando, S., Morellato, A., Cimino, I., Angelini, C., Giacobini, P., Oleari, R., et al. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.744693 · Cited by 1 · see citing works
Stafford, D. E. J. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-818872-9.00058-3 · Cited by 1 · see citing works
Central Hypogonadism in the Male: Physiopathology, Diagnosis and Treatment
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Central Hypogonadism in the Male: Physiopathology, Diagnosis, and Treatment
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Roberts, S. A., & Stafford, D. E. J. (2024) · Springer eBooks · doi:10.1007/978-3-031-66296-6_24
- Authors
- Chan, Y.-M., Lippincott, M. F., Butler, J. P., Sidhoum, V. F., Li, C. X., Plummer, L., & Seminara, S. B.
- Affiliations
- Boston Children's Hospital (US)
- Harvard University (US)
- Brigham and Women's Hospital (US)
- Corresponding author
- Seminara, Stephanie B.
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2014-12-01
- Volume
- 99
- Issue
- 12
- Pages
- E2762-E2771
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- PMC
- PMC4255107
- OpenAlex
- W2169232963
- Cited by
- 39
- References
- 60
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 5 · 2020: 2 · 2019: 4 · 2018: 6 · 2017: 3 · 2016: 1 · 2015: 2
- FWCI
- 2.42
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Doris Duke Charitable Foundation (2013110)
- Massachusetts General Hospital
- Harvard Catalyst
- National Institutes of Health (UL1TR000170)
- National Heart, Lung, and Blood Institute (HL 102923, HL-102924, HL-296 103010, RC2HL102926, RC2HL102923, UC2HL102924, HL-295102925, UC2HL102923, RC2HL102924, UC2HL102926, HL-102926)
- National Institute of Diabetes and Digestive and Kidney Diseases (T32DK007028)
- National Center for Research Resources (UL1RR025758)
- NIH Clinical Center
- National Center for Advancing Translational Sciences
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD043341, F32HD078083, HD052896, P30HD028138, P50HD028138, K24HD067388, U54HD028138, K12HD052896)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- idiopathic hypogonadotropic hypogonadism, kisspeptin, luteinizing hormone secretion, KAL1, FGFR1, PROKR2, GnRH receptor, pubertal development
- MeSH terms
- Adult, Female, Follicle Stimulating Hormone, Humans, Hypogonadism, Luteinizing Hormone, Gonadotropin-Releasing Hormone, Male, Middle Aged, Nerve Net, Nerve Tissue Proteins, Neurons, Receptors, LHRH, Extracellular Matrix Proteins, Young Adult, Kisspeptins
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