ArticleEndocrinology2021
Reproductive Deficits Induced by Prenatal Antimüllerian Hormone Exposure Require Androgen Receptor in Kisspeptin Cells.
Article in Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- GnRH-receptor antagonism as a targeted approach to reproductive dysfunction in polycystic ovary syndrome.EBioMedicine · 2026Article
- Neuroendocrine mechanisms responsible for elevated gonadotrophin-releasing hormone and luteinising hormone pulses in polycystic ovary syndrome.Journal of neuroendocrinology · 2025Review
- POLYCYSTIC OVARY SYNDROME: ORIGINS AND IMPLICATIONS: Gestational anti-Müllerian hormone and testosterone excess combined with maternal adiposity program for polycystic ovary syndrome.Reproduction (Cambridge, England) · 2025Review
- Comparative Analysis of GnRH Pulse Generator Activity in Intact and Gonadectomized Male and Female Mice.Endocrinology · 2025Article
- Androgen Inhibition of Reproductive Neuroendocrine Function in Females and Transgender Males.Endocrinology · 2024Review
- Beyond defence: Immune architects of ovarian health and disease.Seminars in immunopathology · 2024Review
- Investigating GABA Neuron-Specific Androgen Receptor Knockout in two Hyperandrogenic Models of PCOS.Endocrinology · 2024Article
- Anti-Müllerian Hormone: A Molecular Key to Unlocking Polycystic Ovary Syndrome?Seminars in reproductive medicine · 2024Review
- Reproductive Profile of Neuronal Androgen Receptor Knockout Female Mice With a Low Dose of DHT.Endocrinology · 2024Article
- Functional analysis of rare anti-Müllerian hormone protein-altering variants identified in women with PCOS.Molecular human reproduction · 2023Article
- Deletion of Androgen Receptor in LepRb Cells Improves Estrous Cycles in Prenatally Androgenized Mice.Endocrinology · 2023Article
- Update on Animal Models of Polycystic Ovary Syndrome.Endocrinology · 2022Article
- Impaired steroid hormone feedback in polycystic ovary syndrome: Evidence from preclinical models for abnormalities within central circuits controlling fertility.Clinical endocrinology · 2022Review
- Female sexual behavior is disrupted in a preclinical mouse model of PCOS via an attenuated hypothalamic nitric oxide pathway.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Deletion of the homeodomain gene Six3 from kisspeptin neurons causes subfertility in female mice.Molecular and cellular endocrinology · 2022Article
- Cholesterol-lowering effects of taurine through the reduction of ileal FXR signaling due to the alteration of ileal bile acid composition.Amino acids · 2021Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Polycystic ovary syndrome (PCOS) is a common reproductive disorder characterized by elevated androgens and antimüllerian hormone (AMH). These hormones remain elevated throughout pregnancy, and potential effects of hormone exposure on offspring from women with PCOS remain largely unexplored. Expanding on recent reports of prenatal AMH exposure in mice, we have fully characterized the reproductive consequences of prenatal AMH (pAMH) exposure throughout the lifespan of first- and second-generation offspring of both sexes. We also sought to elucidate mechanisms underlying pAMH-induced reproductive effects. There is a known reciprocal relationship between AMH and androgens, and in PCOS and PCOS-like animal models, androgen feedback is dysregulated at the level of the hypothalamus. Kisspeptin neurons express androgen receptors and play a critical role in sexual development and function. We therefore hypothesized that pAMH-induced reproductive phenotypes would be mediated by androgen signaling at the level of kisspeptin cells. We tested the pAMH model in kisspeptin-specific androgen receptor knockout (KARKO) mice and found that virtually all pAMH-induced phenotypes assayed are eliminated in KARKO offspring compared to littermate controls. By demonstrating the necessity of androgen receptor in kisspeptin cells to induce pAMH phenotypes, we have advanced understanding of the interactions between AMH and androgens in the context of prenatal exposure, which could have significant implications for children of women with PCOS.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.