Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (786 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A major gonadotropin secreted by the adenohypophysis (pituitary gland, anterior). Luteinizing hormone regulates steroid production by the interstitial cells of the testis and the ovary. The preovulatory luteinizing hormone surge in females induces ovulation, and subsequent luteinization of the follicle. luteinizing hormone consists of two noncovalently linked subunits, alpha and beta. Within a species, the alpha subunit is common in the three pituitary glycoprotein hormones (TSH, LH and FSH), but the beta subunit is unique and confers its biological specificity.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Hormone, Luteinizing; ICSH (Interstitial Cell Stimulating Hormone); Interstitial Cell-Stimulating Hormone; Hormone, Interstitial Cell-Stimulating; Interstitial Cell Stimulating Hormone; LH (Luteinizing Hormone); Lutropin; Luteozyman.
Where it fits in the MeSH classification
- Broader topics
- Gonadotropins, Pituitary
- Narrower topics
- Glycoprotein Hormones, alpha Subunit; Luteinizing Hormone, beta Subunit
- See also
- Receptors, LH
Related concepts
- Pituitary Gland
- Anterior
- Testis
- Ovary
- Luteinizing Hormone
- Ovulation
- Luteinization
Research landscape
PubMed indexes 49,508 records tagged with the MeSH heading “Luteinizing Hormone” (counts retrieved 2026-10-31). 2,713 of them (5.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 34,650 records.
Reviews account for 2,816 records (5.7%) and meta-analyses for 118. Randomized controlled trials number 1,424 (2.9%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 34,650 |
| 2000-2009 | 7,139 |
| 2010-2019 | 5,006 |
| 2020 onward | 2,713 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,816 | 5.7% |
| Meta-analyses | 118 | 0.2% |
| Randomized controlled trials | 1,424 | 2.9% |
Method: PubMed query "Luteinizing Hormone"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The Roles of Luteinizing Hormone, Follicle-Stimulating Hormone and Testosterone in Spermatogenesis and Folliculogenesis Revisited | 2021 | Review article Design not recorded in structured metadata | 197 | cc by PMID 34884539 · DOI · PMC8658012 |
| Different dendritic domains of the GnRH neuron underlie the pulse and surge modes of GnRH secretion in female mice | 2020 | Research article Design not recorded in structured metadata | 65 | cc by PMID 32644040 · DOI · PMC7347383 |
| Kisspeptin and LH pulsatile temporal coupling in PCOS patients | 2018 | Research article Design not recorded in structured metadata | 61 | cc by PMID 29728876 · DOI · PMC5997113 |
| Metabolic control of luteinizing hormone-responsive ovarian steroidogenesis | 2025 | Research article Design not recorded in structured metadata | 13 | cc by PMID 39615688 · DOI · PMC11732475 |
The Roles of Luteinizing Hormone, Follicle-Stimulating Hormone and Testosterone in Spermatogenesis and Folliculogenesis Revisited [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Spermatogenesis and folliculogenesis involve cell-cell interactions and gene expression orchestrated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH).
- Closing excerpt
- These results should prompt the reassessment of the role of gonadotropins in spermatogenesis, folliculogenesis and therapeutic applications in human hypogonadism and infertility.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (236 words)
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.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34884539 · DOI · PMC8658012
Different dendritic domains of the GnRH neuron underlie the pulse and surge modes of GnRH secretion in female mice [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The gonadotropin-releasing hormone (GnRH) neurons exhibit pulse and surge modes of activity to control fertility.
- Closing excerpt
- These observations indicate that electrical activity at the soma-proximal dendrites of the GnRH neuron is only essential for the LH surge while the distal dendron represents an autonomous zone where synaptic integration drives pulsatile GnRH secretion.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (151 words)
The gonadotropin-releasing hormone (GnRH) neurons exhibit pulse and surge modes of activity to control fertility. They also exhibit an unusual bipolar morphology comprised of a classical soma-proximal dendritic zone and an elongated secretory process that can operate as both a dendrite and an axon, termed a 'dendron'. We show using expansion microscopy that the highest density of synaptic inputs to a GnRH neuron exists at its distal dendron. In vivo, selective chemogenetic inhibition of the GnRH neuron distal dendron abolishes the luteinizing hormone (LH) surge and markedly dampens LH pulses. In contrast, inhibitory chemogenetic and optogenetic strategies targeting the GnRH neuron soma-proximal dendritic zone abolish the LH surge but have no effect upon LH pulsatility. These observations indicate that electrical activity at the soma-proximal dendrites of the GnRH neuron is only essential for the LH surge while the distal dendron represents an autonomous zone where synaptic integration drives pulsatile GnRH secretion.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32644040 · DOI · PMC7347383
Kisspeptin and LH pulsatile temporal coupling in PCOS patients [3]
Abstract reading summary — source excerpts
- Opening excerpt
- PurposeTo evaluate the temporal coupling between spontaneous kisspeptin and luteinizing hormone (LH) pulsatile releases in polycystic ovary syndrome (PCOS) patients.
- Closing excerpt
- This data supports the hypothesis that neuroendocrine impairments in PCOS affect the coupling of kisspeptin with LH pulses and potentially worsen as the disease progresses, becoming unequivocally evident in oligomenorrheic PCOS patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (232 words)
PurposeTo evaluate the temporal coupling between spontaneous kisspeptin and luteinizing hormone (LH) pulsatile releases in polycystic ovary syndrome (PCOS) patients.MethodsWe examined 71 patients diagnosed with PCOS. A 2 h pulsatility study was performed to evaluate serum kisspeptin and LH pulse frequency and concentration, sampled every 10 min; baseline follicle-stimulating hormone (FSH), estradiol (E2), prolactin (PRL), cortisol, 17-hydroksy-progesterone (17OHP), testosterone (T), free testosterone index (FTI, and insulin levels were also measured. Detect and Specific Concordance (SC) algorithms were used to evaluate the temporal coupling associations between spontaneous episodic secretion of kisspeptin and LH.ResultsAll PCOS patients demonstrated LH and kisspeptin pulsatile secretions. When the SC index was calculated across the sample of PCOS patients (n = 71), no temporal coupling was observed between kisspeptin and LH pulses. When PCOS patients were subdivided according to their menstrual cyclicity, oligomenorrheic patients demonstrated elevated kisspeptin pulse frequency. Additionally, the SC index reveled a temporal coupling between kisspeptin and LH secretory peaks only in eumenorrheic patients (n = 30, intermenstrual interval 45 days) did not demonstrate temporal coupling between kisspeptin and LH secretory peaks.ConclusionsThe study of the endogenous kisspeptin and LH pulsatile release revealed the temporal coupling of kisspeptin with LH secretory pulses only in eumenorrheic. This data supports the hypothesis that neuroendocrine impairments in PCOS affect the coupling of kisspeptin with LH pulses and potentially worsen as the disease progresses, becoming unequivocally evident in oligomenorrheic PCOS patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29728876 · DOI · PMC5997113
Metabolic control of luteinizing hormone-responsive ovarian steroidogenesis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- The pituitary gonadotropin luteinizing hormone (LH) is the primary stimulus for ovulation, luteal formation, and progesterone synthesis, regardless of species.
- Closing excerpt
- Understanding hormonal control of metabolic pathways in steroidogenic cells may help elucidate approaches for improving ovarian function and successful reproduction or identifying metabolic targets for developing nonhormonal contraceptives.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (167 words)
The pituitary gonadotropin luteinizing hormone (LH) is the primary stimulus for ovulation, luteal formation, and progesterone synthesis, regardless of species. Despite increased awareness of intracellular signaling events initiating the massive production of progesterone during the reproductive cycle and pregnancy, critical gaps exist in our knowledge of the metabolic and lipidomic pathways required for initiating and maintaining luteal progesterone synthesis. Using untargeted metabolomics and metabolic flux analysis in primary steroidogenic luteal cells, evidence is provided for rapid LHCGR-stimulation of metabolic pathways leading to increased glycolysis and oxygen consumption. Treatment with LH stimulated posttranslational modifications of enzymes involved in de novo lipogenesis. Mechanistic studies implicated a crucial role for de novo fatty acid synthesis and fatty acid oxidation in energy homeostasis, LHCGR/PKA signaling, and, consequently, progesterone production. These findings reveal novel hormone-sensitive metabolic pathways essential for maintaining LHCGR/PKA signaling and steroidogenesis. Understanding hormonal control of metabolic pathways in steroidogenic cells may help elucidate approaches for improving ovarian function and successful reproduction or identifying metabolic targets for developing nonhormonal contraceptives.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39615688 · DOI · PMC11732475
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Ovulation: Parallels With Inflammatory Processes [5]
- Research article Hypopituitarism [6]
- Research article The Gonadotropin-Releasing Hormone Pulse Generator [7]
- Research article Coordination of Ovulation and Oocyte Maturation: A Good Egg at the Right Time [8]
- Research article GnRH pulse frequency-dependent differential regulation of LH and FSH gene expression [9]
- Research article On the control of gonadotropin secretion in the rhesus monkey [10]
References
- Oduwole OO, Huhtaniemi IT, Misrahi M. The Roles of Luteinizing Hormone, Follicle-Stimulating Hormone and Testosterone in Spermatogenesis and Folliculogenesis Revisited. . 2021. PMID 34884539 · DOI · PMC8658012
- Wang L, Guo W, Shen X, Yeo S, Long H, Wang Z, et al.. Different dendritic domains of the GnRH neuron underlie the pulse and surge modes of GnRH secretion in female mice. . 2020. PMID 32644040 · DOI · PMC7347383
- Katulski K, Podfigurna A, Czyzyk A, Meczekalski B, Genazzani AD. Kisspeptin and LH pulsatile temporal coupling in PCOS patients. . 2018. PMID 29728876 · DOI · PMC5997113
- Przygrodzka E, Bhinderwala F, Powers R, McFee RM, Cupp AS, Wood JR, et al.. Metabolic control of luteinizing hormone-responsive ovarian steroidogenesis. . 2025. PMID 39615688 · DOI · PMC11732475
- Duffy DM, Ko C, Jo M, Brannstrom M, Curry TE. Ovulation: Parallels With Inflammatory Processes. Endocr Rev. 2019. PMID 30496379 · DOI · PMC6405411
- Schneider HJ, Aimaretti G, Kreitschmann-Andermahr I, Stalla GK, Ghigo E. Hypopituitarism. Lancet. 2007. PMID 17467517 · DOI
- Herbison AE. The Gonadotropin-Releasing Hormone Pulse Generator. Endocrinology. 2018. PMID 30272161 · DOI
- Robker RL, Hennebold JD, Russell DL. Coordination of Ovulation and Oocyte Maturation: A Good Egg at the Right Time. Endocrinology. 2018. PMID 30010832 · DOI · PMC6456964
- Thompson IR, Kaiser UB. GnRH pulse frequency-dependent differential regulation of LH and FSH gene expression. Mol Cell Endocrinol. 2014. PMID 24056171 · DOI · PMC3947649
- Knobil E. On the control of gonadotropin secretion in the rhesus monkey. Recent Prog Horm Res. 1974. PMID 4210416 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.