{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,9]],"date-time":"2026-05-09T08:18:38Z","timestamp":1778314718901,"version":"3.51.4"},"reference-count":63,"publisher":"The Endocrine Society","issue":"2","license":[{"start":{"date-parts":[[2025,6,20]],"date-time":"2025-06-20T00:00:00Z","timestamp":1750377600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100009633","name":"Eunice Kennedy Shriver National Institute of Child Health and Human Development","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100009633","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,1,21]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Context<\/jats:title>\n                    <jats:p>Daughters of women with polycystic ovary syndrome (PCOS-d) and girls with overweight\/obesity (OW-g) have hyperandrogenemia (HA) beginning in childhood. However, other features of their early reproductive phenotypes differ, suggesting that there are distinct mechanisms conferring increased risk for PCOS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>We performed a cross-sectional study of adolescent girls during the early postmenarchal transition.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Design, Setting, and Participants<\/jats:title>\n                    <jats:p>PCOS-d (n = 15), OW-g (n = 12), and lean control girls (LC; n = 17) were studied within .2 to 1.2\u2005 years of menarche. Metabolic and reproductive phenotypes were assessed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>SHBG levels were lower (P &amp;lt; .0001) in PCOS-d and OW-g vs LC. Free testosterone levels were higher (P = .02) in OW-g vs LC. dehydroepiandrosterone sulfate levels were higher (P = .04) in PCOS-d vs LC and trended higher in OW-g vs LC (P = .07). Morning LH levels were higher in PCOS-d vs OW-g (P = .02). LH and FSH responses to GnRH analog were also increased in PCOS-d vs OW-g (LH area under the curve (AUC) P = .006, FSH AUC P = .01). The prevalence of HA was similarly increased in PCOS-d and OW-g vs LC (\u03c72 \u00a0P = .04). The prevalence of ovulatory dysfunction (menses &amp;gt;45\u2005days or &amp;lt;21\u2005days) was increased (\u03c72 \u00a0P = .05) in PCOS-d vs OW-g and LC.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Both PCOS-d and OW-g had persistent HA during the early postmenarchal transition. However, ovulatory dysfunction and neuroendocrine abnormalities, elevated basal, and stimulated LH responses to GnRH analog were observed only in PCOS-d. These findings support the existence of distinct developmental trajectories leading to polycystic ovary syndrome, with early neuroendocrine dysregulation in PCOS-d and peripheral, likely adiposity-related, androgen excess in OW-g.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1210\/clinem\/dgaf363","type":"journal-article","created":{"date-parts":[[2025,6,19]],"date-time":"2025-06-19T08:01:47Z","timestamp":1750320107000},"page":"553-560","source":"Crossref","is-referenced-by-count":1,"title":["The Ontogeny of Distinct Reproductive Phenotypes in Girls at Risk for PCOS During the Postmenarchal Transition"],"prefix":"10.1210","volume":"111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2468-7137","authenticated-orcid":false,"given":"Laura C","family":"Torchen","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Ann & Robert H Lurie Children's Hospital of Chicago, Feinberg School of Medicine, Northwestern University , Chicago, IL 60611 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