{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:41:55Z","timestamp":1791276115744,"version":"4.1.0"},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2016,1,11]],"date-time":"2016-01-11T00:00:00Z","timestamp":1452470400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["P30 AR061313 and R01 AR061376 (to MBD), T32 DK007529, F32 AR065386, and K08 AR067854"],"award-info":[{"award-number":["P30 AR061313 and R01 AR061376 (to MBD), T32 DK007529, F32 AR065386, and K08 AR067854"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,5,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>X-linked hypophosphatemia (XLH) is characterized by impaired renal tubular reabsorption of phosphate owing to increased circulating FGF23 levels, resulting in rickets in growing children and impaired bone mineralization. Increased FGF23 decreases renal brush border membrane sodium-dependent phosphate transporter IIa (Npt2a) causing renal phosphate wasting, impairs 1-\u03b1 hydroxylation of 25-hydroxyvitamin D, and induces the vitamin D 24-hydroxylase, leading to inappropriately low circulating levels of 1,25-dihydroxyvitamin D (1,25D). The goal of therapy is prevention of rickets and improvement of growth in children by phosphate and 1,25D supplementation. However, this therapy is often complicated by hypercalcemia and nephrocalcinosis and does not always prevent hyperparathyroidism. To determine if 1,25D or blocking FGF23 action can improve the skeletal phenotype without phosphate supplementation, mice with XLH (Hyp) were treated with daily 1,25D repletion, FGF23 antibodies (FGF23Ab), or biweekly high-dose 1,25D from d2 to d75 without supplemental phosphate. All treatments maintained normocalcemia, increased serum phosphate, and normalized parathyroid hormone levels. They also prevented the loss of Npt2a, \u03b1-Klotho, and pERK1\/2 immunoreactivity observed in the kidneys of untreated Hyp mice. Daily treatment with 1,25D decreased urine phosphate losses despite a marked increase in bone FGF23 mRNA and in circulating FGF23 levels. Daily 1,25D was more effective than other treatments in normalizing the growth plate and metaphyseal organization. In addition to being the only therapy that normalized lumbar vertebral height and body weight, daily 1,25D therapy normalized bone geometry and was more effective than FGF23Ab in improving trabecular bone structure. Daily 1,25D and FGF23Ab improved cortical microarchitecture and whole-bone biomechanical properties more so than biweekly 1,25D. Thus, monotherapy with 1,25D improves growth, skeletal microarchitecture, and bone strength in the absence of phosphate supplementation despite enhancing FGF23 expression, demonstrating that 1,25D has direct beneficial effects on the skeleton in XLH, independent of its role in phosphate homeostasis. \u00a9 2016 American Society for Bone and Mineral Research.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.2783","type":"journal-article","created":{"date-parts":[[2016,1,11]],"date-time":"2016-01-11T20:39:32Z","timestamp":1452544772000},"page":"929-939","source":"Crossref","is-referenced-by-count":62,"title":["1,25-Dihydroxyvitamin D Alone Improves Skeletal Growth, Microarchitecture, and Strength in a Murine Model of XLH, Despite Enhanced FGF23 Expression"],"prefix":"10.1093","volume":"31","author":[{"given":"Eva S","family":"Liu","sequence":"first","affiliation":[{"name":"Harvard Medical SchoolBostonMAUSA"},{"name":"Endocrine UnitMassachusetts General HospitalBostonMAUSA"},{"name":"Division of Endocrinology, Diabetes, and HypertensionBrigham and Women's HospitalBostonMAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janaina S","family":"Martins","sequence":"additional","affiliation":[{"name":"Division of NephrologyUniversidade de S\u00e3o PauloS\u00e3o PauloBrazil"},{"name":"Harvard Medical SchoolBostonMAUSA"},{"name":"Endocrine UnitMassachusetts General HospitalBostonMAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adalbert","family":"Raimann","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Adolescent MedicineMedical University ViennaViennaAustria"},{"name":"Harvard Medical SchoolBostonMAUSA"},{"name":"Endocrine UnitMassachusetts General HospitalBostonMAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Byongsoo Timothy","family":"Chae","sequence":"additional","affiliation":[{"name":"Endocrine UnitMassachusetts General HospitalBostonMAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel J","family":"Brooks","sequence":"additional","affiliation":[{"name":"Department of OrthopedicsBeth Israel Deaconess Medical CenterBostonMAUSA"},{"name":"Endocrine UnitMassachusetts General HospitalBostonMAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vanda","family":"Jorgetti","sequence":"additional","affiliation":[{"name":"Division of NephrologyUniversidade de S\u00e3o PauloS\u00e3o PauloBrazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary L","family":"Bouxsein","sequence":"additional","affiliation":[{"name":"Department of OrthopedicsBeth Israel Deaconess Medical CenterBostonMAUSA"},{"name":"Harvard Medical SchoolBostonMAUSA"},{"name":"Endocrine UnitMassachusetts General HospitalBostonMAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie B","family":"Demay","sequence":"additional","affiliation":[{"name":"Harvard Medical SchoolBostonMAUSA"},{"name":"Endocrine UnitMassachusetts General HospitalBostonMAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2016,1,11]]},"reference":[{"issue":"7","key":"2024021014182712600_jbmr2783-bib-0001","doi-asserted-by":"crossref","first-page":"1381","DOI":"10.1002\/jbmr.340","article-title":"A clinician's guide to X-linked hypophosphatemia","volume":"26","author":"Carpenter","year":"2011","journal-title":"J Bone Miner Res"},{"issue":"4","key":"2024021014182712600_jbmr2783-bib-0002","first-page":"839","article-title":"Effects of calcitriol and phosphorus therapy on the growth of patients with X-linked hypophosphatemia","volume":"76","author":"Friedman","year":"1993","journal-title":"J Clin Endocrinol Metab"},{"issue":"1","key":"2024021014182712600_jbmr2783-bib-0003","doi-asserted-by":"crossref","first-page":"E38","DOI":"10.1152\/ajpendo.00008.2006","article-title":"Pathogenic role of Fgf23 in Hyp mice","volume":"291","author":"Liu","year":"2006","journal-title":"Am J Physiol Endocrinol Metab"},{"issue":"2)","key":"2024021014182712600_jbmr2783-bib-0004","first-page":"130","article-title":"A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets","volume":"11","year":"1995","journal-title":"The HYP Consortium. 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