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However, the mechanisms by which\n                    <jats:italic>DLK1<\/jats:italic>\n                    influences pubertal timing remain unclear. We investigated pubertal timing in\n                    <jats:italic>Dlk1<\/jats:italic>\n                    knockout (KO) mice with either global or selective central nervous system (CNS) deletion of\n                    <jats:italic>Dlk1<\/jats:italic>\n                    , compared with control mice. Puberty onset and body weight were assessed, along with potential mediators of pubertal timing, including leptin and kisspeptin.\n                    <jats:italic>Dlk1<\/jats:italic>\n                    KO females reached puberty at the same age as controls, despite lower body weight.\n                    <jats:italic>Dlk1<\/jats:italic>\n                    KO males had delayed preputial separation but, like females, reached puberty at significantly lower body weight. Serum leptin and hypothalamic\n                    <jats:italic>Socs3<\/jats:italic>\n                    mRNA, a downstream leptin effector, were lower peri\u2010pubertally in\n                    <jats:italic>Dlk1<\/jats:italic>\n                    KO females than in controls.\n                    <jats:italic>Kiss1<\/jats:italic>\n                    mRNA levels in the mediobasal hypothalamus were significantly lower in\n                    <jats:italic>Dlk1<\/jats:italic>\n                    KO females at puberty onset. Selective\n                    <jats:italic>Dlk1<\/jats:italic>\n                    deletion in neurons and glial cells did not affect pubertal timing. These findings suggest that peripheral sources of Dlk1 contribute to the metabolic and endocrine regulation of pubertal timing. The absence of Dlk1 appears to alter the metabolic milieu in which puberty occurs, allowing activation of the reproductive axis despite low body weight and reduced hypothalamic kisspeptin expression.\n                  <\/jats:p>","DOI":"10.1111\/jne.70248","type":"journal-article","created":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T09:37:06Z","timestamp":1788255426000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Dlk1\u2010deficient mice achieve puberty despite low body weight and low levels of leptin and kisspeptin"],"prefix":"10.1111","volume":"38","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6711-6097","authenticated-orcid":false,"given":"Delanie B.","family":"Macedo","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Diabetes and Hypertension Brigham and Women's Hospital and Harvard Medical School  Boston Massachusetts USA"},{"name":"Integrated Medical Care Center, Center for Health Sciences University of Fortaleza  Fortaleza Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7937-2952","authenticated-orcid":false,"given":"Sidney A.","family":"Pereira","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Hypertension Brigham and Women's Hospital and Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meijiao","family":"Wang","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Hypertension Brigham and Women's Hospital and Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Physiology, School of Basic Medicine Chongqing Medical University  Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Han Kim","family":"Kyeol","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Hypertension Brigham 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