{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T08:15:25Z","timestamp":1791101725353,"version":"4.1.0"},"reference-count":68,"publisher":"The Endocrine Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Pubertal onset only occurs in a favorable, anabolic hormonal environment. The neuropeptide kisspeptin, encoded by the Kiss1 gene, modifies GnRH neuronal activity to initiate puberty and maintain fertility, but the factors that regulate Kiss1 neurons and permit pubertal maturation remain to be clarified. The anabolic factor insulin may signal nutritional status to these neurons. To determine whether insulin sensing plays an important role in Kiss1 neuron function, we generated mice lacking insulin receptors in Kiss1 neurons (IR\u0394Kiss mice). IR\u0394Kiss females showed a delay in vaginal opening and in first estrus, whereas IR\u0394Kiss males also exhibited late sexual maturation. Correspondingly, LH levels in IR\u0394Kiss mice were reduced in early puberty in both sexes. Adult reproductive capacity, body weight, fat composition, food intake, and glucose regulation were comparable between the 2 groups. These data suggest that impaired insulin sensing by Kiss1 neurons delays the initiation of puberty but does not affect adult fertility. These studies provide insight into the mechanisms regulating pubertal timing in anabolic states.<\/jats:p>","DOI":"10.1210\/en.2012-2056","type":"journal-article","created":{"date-parts":[[2013,2,8]],"date-time":"2013-02-08T01:27:51Z","timestamp":1360286871000},"page":"1337-1348","source":"Crossref","is-referenced-by-count":101,"title":["Delayed Puberty but Normal Fertility in Mice With Selective Deletion of Insulin Receptors From Kiss1 Cells"],"prefix":"10.1210","volume":"154","author":[{"given":"Xiaoliang","family":"Qiu","sequence":"first","affiliation":[{"name":"Center for Diabetes and Endocrine Research (X.Q., A.R.D., J.S.M., L.D.F., J.W.H.), University of Toledo College of Medicine, Toledo, Ohio 43614"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abigail R.","family":"Dowling","sequence":"first","affiliation":[{"name":"Center for Diabetes and Endocrine Research (X.Q., A.R.D., J.S.M., L.D.F., J.W.H.), University of Toledo College of Medicine, Toledo, Ohio 43614"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph S.","family":"Marino","sequence":"first","affiliation":[{"name":"Center for Diabetes and Endocrine Research (X.Q., A.R.D., J.S.M., L.D.F., J.W.H.), University of Toledo College of Medicine, Toledo, Ohio 43614"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Latrice D.","family":"Faulkner","sequence":"first","affiliation":[{"name":"Center for Diabetes and Endocrine Research (X.Q., A.R.D., J.S.M., L.D.F., J.W.H.), University of Toledo College of Medicine, Toledo, Ohio 43614"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin","family":"Bryant","sequence":"first","affiliation":[{"name":"Chemistry Department (B.B.), Carnegie Mellon University, Pittsburgh, Pennsylvania 15213"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jens C.","family":"Br\u00fcning","sequence":"first","affiliation":[{"name":"Institute for Genetics (J.C.B.), Department of Mouse Genetics 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