{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T01:40:03Z","timestamp":1790127603391,"version":"4.0.1"},"reference-count":48,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2024,2,12]],"date-time":"2024-02-12T00:00:00Z","timestamp":1707696000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001505","name":"Health Research Council of New Zealand","doi-asserted-by":"publisher","award":["18\/671"],"award-info":[{"award-number":["18\/671"]}],"id":[{"id":"10.13039\/501100001505","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Neuroendocrinology"],"published-print":{"date-parts":[[2024,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Excess levels of circulating androgens during prenatal or peripubertal development are an important cause of polycystic ovary syndrome (PCOS), with the brain being a key target. Approximately half of the women diagnosed with PCOS also experience metabolic syndrome; common features including obesity, insulin resistance and hyperinsulinemia. Although a large amount of clinical and preclinical evidence has confirmed this relationship between androgens and the reproductive and metabolic features of PCOS, the mechanisms by which androgens cause this dysregulation are unknown. Neuron\u2010specific androgen receptor knockout alleviates some PCOS\u2010like features in a peripubertal dihydrotestosterone (DHT) mouse model, but the specific neuronal populations mediating these effects are undefined. A candidate population is the agouti\u2010related peptide (AgRP)\u2010expressing neurons, which are important for both reproductive and metabolic function. We used a well\u2010characterised peripubertal androgenized mouse model and Cre\u2010loxP transgenics to investigate whether deleting androgen receptors specifically from AgRP neurons can alleviate the induced reproductive and metabolic dysregulation. Androgen receptors were co\u2010expressed in 66% of AgRP neurons in control mice, but only in &lt;2% of AgRP neurons in knockout mice. The number of AgRP neurons was not altered by the treatments. Only 20% of androgen receptor knockout mice showed rescue of DHT\u2010induced androgen\u2010induced anovulation and acyclicity. Furthermore, androgen receptor knockout did not rescue metabolic dysfunction (body weight, adiposity or glucose and insulin tolerance). While we cannot rule out developmental compensation in our model, these results suggest peripubertal androgen excess does not markedly influence\n                    <jats:italic>Agrp<\/jats:italic>\n                    expression and does not dysregulate reproductive and metabolic function through direct actions of androgens onto AgRP neurons.\n                  <\/jats:p>","DOI":"10.1111\/jne.13370","type":"journal-article","created":{"date-parts":[[2024,2,12]],"date-time":"2024-02-12T05:13:29Z","timestamp":1707714809000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Androgen receptor actions on\n                    <scp>AgRP<\/scp>\n                    neurons are not a major cause of reproductive and metabolic impairments in peripubertally androgenized mice"],"prefix":"10.1111","volume":"36","author":[{"given":"Romy I.","family":"Kerbus","sequence":"first","affiliation":[{"name":"Centre for Neuroendocrinology and Department of Anatomy University of Otago School of Biomedical Sciences  Dunedin New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caroline","family":"Decourt","sequence":"additional","affiliation":[{"name":"Centre for Neuroendocrinology and Department of Anatomy University of Otago School of Biomedical Sciences  Dunedin New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Megan A.","family":"Inglis","sequence":"additional","affiliation":[{"name":"Centre for Neuroendocrinology and Department of Anatomy University of Otago School of Biomedical Sciences  Dunedin New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0309-532X","authenticated-orcid":false,"given":"Rebecca E.","family":"Campbell","sequence":"additional","affiliation":[{"name":"Department of Physiology University of Otago School of Biomedical Sciences  Dunedin New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6747-8047","authenticated-orcid":false,"given":"Greg M.","family":"Anderson","sequence":"additional","affiliation":[{"name":"Centre for Neuroendocrinology and Department of Anatomy University of Otago School of Biomedical Sciences  Dunedin New 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