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Repression of the Wnt\/<jats:italic>\u03b2<\/jats:italic>\u2010catenin signaling pathway is associated with bone abnormalities. Inhibition of glycogen synthase kinase (<jats:styled-content style=\"fixed-case\">GSK<\/jats:styled-content>)\u20103<jats:italic>\u03b2<\/jats:italic>, a critical component of the Wnt\/<jats:italic>\u03b2<\/jats:italic>\u2010catenin signaling pathway, increases bone volume through accumulation of <jats:italic>\u03b2<\/jats:italic>\u2010catenin. It remains unknown whether inhibition of <jats:styled-content style=\"fixed-case\">GSK<\/jats:styled-content>\u20103<jats:italic>\u03b2<\/jats:italic> increases bone volume in <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>. The present in\u00a0vivo study examined the effects of <jats:styled-content style=\"fixed-case\">GSK<\/jats:styled-content>\u20103<jats:italic>\u03b2<\/jats:italic> inhibition on bone volume in <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content> mice. Wild\u2010type mice were divided into three groups. One group was fed a control diet (<jats:styled-content style=\"fixed-case\">CNT<\/jats:styled-content>) and the other two groups were fed a diet containing 0.2% adenine and given water with or without lithium chloride (LiCl), a <jats:styled-content style=\"fixed-case\">GSK<\/jats:styled-content>\u20103 inhibitor (<jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> CKD<\/jats:styled-content>+LiCl, respectively). <jats:styled-content style=\"fixed-case\">GSK<\/jats:styled-content>\u20103<jats:italic>\u03b2<\/jats:italic> heterozygous knockout mice were fed a diet containing 0.2% adenine (<jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">GSK<\/jats:styled-content>\u20103<jats:italic>\u03b2<\/jats:italic><jats:sup>+\/\u2212<\/jats:sup>). After 6\u00a0weeks, trabecular and cortical bone volumes of the femur were analyzed using microcomputed tomography. <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content> mice developed azotemia, hyperphosphatemia, and hyperparathyroidism, followed by a decrease in cortical bone volume without any change in trabecular bone volume. Serum levels of urea nitrogen, phosphate, and parathyroid hormone were comparable among the three groups of <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content> mice. Trabecular bone volume increased in <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">GSK<\/jats:styled-content>\u20103<jats:italic>\u03b2<\/jats:italic><jats:sup>+\/\u2212<\/jats:sup> and <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>+LiCl mice compared with <jats:styled-content style=\"fixed-case\">CNT<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content> mice. However, there were no significant differences in cortical bone volume among the three groups of <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content> mice. The results suggest that inhibition of <jats:styled-content style=\"fixed-case\">GSK<\/jats:styled-content>\u20103<jats:italic>\u03b2<\/jats:italic> increases trabecular bone volume but not cortical bone volume in adenine\u2010induced uremic mice with uncontrolled hyperparathyroidism.<\/jats:p>","DOI":"10.14814\/phy2.13010","type":"journal-article","created":{"date-parts":[[2016,11,2]],"date-time":"2016-11-02T02:54:12Z","timestamp":1478055252000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Inhibition of <scp>GSK<\/scp>\u20103<i>\u03b2<\/i> increases trabecular bone volume but not cortical bone volume in adenine\u2010induced uremic mice with severe hyperparathyroidism"],"prefix":"10.14814","volume":"4","author":[{"given":"Narihito","family":"Tatsumoto","sequence":"first","affiliation":[{"name":"Department of Clinical Pharmacology Faculty of Medical Sciences Kyushu University Fukuoka Japan"},{"name":"Department 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Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masanori","family":"Tokumoto","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Fukuoka Dental College Fukuoka Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazuhiko","family":"Tsuruya","sequence":"additional","affiliation":[{"name":"Department of Medicine and Clinical Science Graduate School of Medical Sciences Kyushu University Fukuoka Japan"},{"name":"Department of Integrated Therapy for Chronic Kidney Disease Graduate School of Medical Sciences Kyushu University Fukuoka Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takanari","family":"Kitazono","sequence":"additional","affiliation":[{"name":"Department of Medicine and Clinical Science Graduate School of Medical Sciences Kyushu University Fukuoka 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