{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T17:13:27Z","timestamp":1793121207164,"version":"4.5.0"},"reference-count":62,"publisher":"The Endocrine Society","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2007,8,1]]},"abstract":"<jats:p>The role of classical genomic androgen receptor (AR) mediated actions in female reproductive physiology remains unclear. Female mice homozygous for an in-frame deletion of exon 3 of the Ar (AR\u2212\/\u2212) were subfertile, exhibiting delayed production of their first litter (AR+\/+ = 22 d vs. AR\u2212\/\u2212 = 61 d, P &amp;lt; 0.05) and producing 60% fewer pups\/litter (AR+\/+: 8.1 \u00b1 0.4 vs. AR\u2212\/\u2212: 3.2 \u00b1 0.9, P &amp;lt; 0.01). Heterozygous females (AR+\/\u2212) exhibited an age-dependent 55% reduction (P &amp;lt; 0.01) in pups per litter, evident from 6 months of age (P &amp;lt; 0.05), compared with AR+\/+, indicating a significant gene dosage effect on female fertility. Ovulation was defective with a significant reduction in corpora lutea numbers (48\u201379%, P &amp;lt; 0.01) in 10- to 12- and 26-wk-old AR+\/\u2212 and AR\u2212\/\u2212 females and a 57% reduction in oocytes recovered from naturally mated AR\u2212\/\u2212 females (AR+\/+: 9.8 \u00b1 1.0 vs. AR\u2212\/\u2212: 4.2 \u00b1 1.2, P &amp;lt; 0.01); however, early embryo development to the two-cell stage was unaltered. The delay in first litter, reduction in natural ovulation rate, and aromatase expression in AR+\/\u2212 and AR\u2212\/\u2212 ovaries, coupled with the restored ovulation rate by gonadotropin hyperstimulation in AR\u2212\/\u2212 females, suggest aberrant gonadotropin regulation. A 2.7-fold increase (AR+\/+: 35.4 \u00b1 13.4 vs. AR\u2212\/\u2212: 93.9 \u00b1 6.1, P &amp;lt; 0.01) in morphologically unhealthy antral follicles demonstrated deficiencies in late follicular development, although growing follicle populations and growth rates were unaltered. This novel model reveals that classical genomic AR action is critical for normal ovarian function, although not for follicle depletion and that haploinsufficiency for an inactivated AR may contribute to a premature reduction in female fecundity.<\/jats:p>","DOI":"10.1210\/en.2007-0248","type":"journal-article","created":{"date-parts":[[2007,4,26]],"date-time":"2007-04-26T20:48:27Z","timestamp":1177620507000},"page":"3674-3684","source":"Crossref","is-referenced-by-count":132,"title":["Female Mice Haploinsufficient for an Inactivated Androgen Receptor (AR) Exhibit Age-Dependent Defects That Resemble the AR Null Phenotype of Dysfunctional Late Follicle Development, Ovulation, and Fertility"],"prefix":"10.1210","volume":"148","author":[{"given":"K. A.","family":"Walters","sequence":"first","affiliation":[{"name":"Department of Andrology (K.A.W., C.M.A., M.J., P.R.L., D.J.H.), ANZAC Research Institute, Concord Hospital, University of Sydney, New South Wales 2139, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. M.","family":"Allan","sequence":"additional","affiliation":[{"name":"Department of Andrology (K.A.W., C.M.A., M.J., P.R.L., D.J.H.), ANZAC Research Institute, Concord Hospital, University of Sydney, New South Wales 2139, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Jimenez","sequence":"additional","affiliation":[{"name":"Department of Andrology (K.A.W., C.M.A., M.J., P.R.L., D.J.H.), ANZAC Research Institute, Concord Hospital, University of Sydney, New South Wales 2139, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. R.","family":"Lim","sequence":"additional","affiliation":[{"name":"Department of Andrology (K.A.W., C.M.A., M.J., P.R.L., D.J.H.), ANZAC Research Institute, Concord Hospital, University of Sydney, New South Wales 2139, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. A.","family":"Davey","sequence":"additional","affiliation":[{"name":"Department of Medicine (R.A.D., J.D.Z.), University of Melbourne, Austin Health, Heidelberg 3084, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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