{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T18:07:20Z","timestamp":1792606040389,"version":"4.5.0"},"reference-count":667,"publisher":"The Endocrine Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2008,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The vitamin D endocrine system is essential for calcium and bone homeostasis. The precise mode of action and the full spectrum of activities of the vitamin D hormone, 1,25-dihydroxyvitamin D [1,25-(OH)2D], can now be better evaluated by critical analysis of mice with engineered deletion of the vitamin D receptor (VDR). Absence of a functional VDR or the key activating enzyme, 25-OHD-1\u03b1-hydroxylase (CYP27B1), in mice creates a bone and growth plate phenotype that mimics humans with the same congenital disease or severe vitamin D deficiency. The intestine is the key target for the VDR because high calcium intake, or selective VDR rescue in the intestine, restores a normal bone and growth plate phenotype.<\/jats:p><jats:p>The VDR is nearly ubiquitously expressed, and almost all cells respond to 1,25-(OH)2D exposure; about 3% of the mouse or human genome is regulated, directly and\/or indirectly, by the vitamin D endocrine system, suggesting a more widespread function. VDR-deficient mice, but not vitamin D- or 1\u03b1-hydroxylase-deficient mice, and man develop total alopecia, indicating that the function of the VDR and its ligand is not fully overlapping. The immune system of VDR- or vitamin D-deficient mice is grossly normal but shows increased sensitivity to autoimmune diseases such as inflammatory bowel disease or type 1 diabetes after exposure to predisposing factors. VDR-deficient mice do not have a spontaneous increase in cancer but are more prone to oncogene- or chemocarcinogen-induced tumors. They also develop high renin hypertension, cardiac hypertrophy, and increased thrombogenicity. Vitamin D deficiency in humans is associated with increased prevalence of diseases, as predicted by the VDR null phenotype. Prospective vitamin D supplementation studies with multiple noncalcemic endpoints are needed to define the benefits of an optimal vitamin D status.<\/jats:p>","DOI":"10.1210\/er.2008-0004","type":"journal-article","created":{"date-parts":[[2008,10,8]],"date-time":"2008-10-08T21:52:41Z","timestamp":1223502761000},"page":"726-776","source":"Crossref","is-referenced-by-count":1425,"title":["Vitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice"],"prefix":"10.1210","volume":"29","author":[{"given":"Roger","family":"Bouillon","sequence":"first","affiliation":[{"name":"Katholieke Universiteit Leuven, Laboratory of Experimental Medicine and Endocrinology (R.B., G.C., L.V., E.v.E., A.V., L.L., C.M.), 3000 Leuven, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Geert","family":"Carmeliet","sequence":"first","affiliation":[{"name":"Katholieke Universiteit Leuven, Laboratory of Experimental Medicine and Endocrinology (R.B., G.C., L.V., E.v.E., A.V., L.L., C.M.), 3000 Leuven, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lieve","family":"Verlinden","sequence":"first","affiliation":[{"name":"Katholieke Universiteit Leuven, Laboratory of Experimental Medicine and Endocrinology (R.B., G.C., L.V., E.v.E., A.V., L.L., C.M.), 3000 Leuven, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Evelyne","family":"van Etten","sequence":"first","affiliation":[{"name":"Katholieke Universiteit Leuven, Laboratory of Experimental Medicine and Endocrinology (R.B., G.C., L.V., E.v.E., A.V., L.L., C.M.), 3000 Leuven, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annemieke","family":"Verstuyf","sequence":"first","affiliation":[{"name":"Katholieke Universiteit Leuven, Laboratory of Experimental Medicine and Endocrinology (R.B., G.C., L.V., E.v.E., A.V., L.L., C.M.), 3000 Leuven, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hilary 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