Tags

Type your tag names separated by a space and hit enter

Vitamin D resistance.
Best Pract Res Clin Endocrinol Metab. 2006 Dec; 20(4):627-45.BP

Abstract

Vitamin D is a secosteroid of nutritional origin but can also be generated in the skin by ultraviolet light. After two hydroxylations 1,25-(OH)2 vitamin D avidly binds and activates the vitamin D receptor (VDR), a nuclear transcription factor, hereby regulating a large number of genes. The generation of VDR deficient mice has expanded the knowledge on vitamin D from a calcium-regulating hormone to a humoral factor with extensive actions. The effects of the vitamin D system on calcium and bone homeostasis are largely mediated by promoting active intestinal calcium transport via the induction of the epithelial calcium channel TRPV6. Although VDR is redundant in bone, it may regulate the differentiation and function of several bone cells. In skin, VDR expression in keratinocytes is essential in a ligand-independent manner for the maintenance of the normal hair cycle. Therefore, VDR but not vitamin D deficiency results in alopecia. Moreover, 1,25-(OH)2 vitamin D impairs the proliferation not only of keratinocytes but also of many cell types by regulating the expression of cell cycle genes, leading to a G1 cell cycle arrest. In addition, VDR inactivation in mice results in high renin hypertension, cardiac hypertrophy and thrombogenesis. Finally, a dual effect of vitamin D was observed in the immune system where it stimulates the innate immune system while tapering down excessive activation of the acquired immune system. Taken together, the vitamin D endocrine system not only regulates calcium homeostasis but affects several systems mainly by altering gene expression but also by ligand-independent actions.

Authors+Show Affiliations

Laboratory for Experimental Medicine and Endocrinology, Campus Gasthuisberg, Onderwijs & Navorsing 1, Herestraat 49, bus 902, B-3000 Leuven, Belgium. Roger.Bouillon@med.kuleuven.beNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

17161336

Citation

Bouillon, Roger, et al. "Vitamin D Resistance." Best Practice & Research. Clinical Endocrinology & Metabolism, vol. 20, no. 4, 2006, pp. 627-45.
Bouillon R, Verstuyf A, Mathieu C, et al. Vitamin D resistance. Best Pract Res Clin Endocrinol Metab. 2006;20(4):627-45.
Bouillon, R., Verstuyf, A., Mathieu, C., Van Cromphaut, S., Masuyama, R., Dehaes, P., & Carmeliet, G. (2006). Vitamin D resistance. Best Practice & Research. Clinical Endocrinology & Metabolism, 20(4), 627-45.
Bouillon R, et al. Vitamin D Resistance. Best Pract Res Clin Endocrinol Metab. 2006;20(4):627-45. PubMed PMID: 17161336.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vitamin D resistance. AU - Bouillon,Roger, AU - Verstuyf,Annemieke, AU - Mathieu,Chantal, AU - Van Cromphaut,Sophie, AU - Masuyama,Ritsuko, AU - Dehaes,Petra, AU - Carmeliet,Geert, PY - 2006/12/13/pubmed PY - 2007/2/7/medline PY - 2006/12/13/entrez SP - 627 EP - 45 JF - Best practice & research. Clinical endocrinology & metabolism JO - Best Pract. Res. Clin. Endocrinol. Metab. VL - 20 IS - 4 N2 - Vitamin D is a secosteroid of nutritional origin but can also be generated in the skin by ultraviolet light. After two hydroxylations 1,25-(OH)2 vitamin D avidly binds and activates the vitamin D receptor (VDR), a nuclear transcription factor, hereby regulating a large number of genes. The generation of VDR deficient mice has expanded the knowledge on vitamin D from a calcium-regulating hormone to a humoral factor with extensive actions. The effects of the vitamin D system on calcium and bone homeostasis are largely mediated by promoting active intestinal calcium transport via the induction of the epithelial calcium channel TRPV6. Although VDR is redundant in bone, it may regulate the differentiation and function of several bone cells. In skin, VDR expression in keratinocytes is essential in a ligand-independent manner for the maintenance of the normal hair cycle. Therefore, VDR but not vitamin D deficiency results in alopecia. Moreover, 1,25-(OH)2 vitamin D impairs the proliferation not only of keratinocytes but also of many cell types by regulating the expression of cell cycle genes, leading to a G1 cell cycle arrest. In addition, VDR inactivation in mice results in high renin hypertension, cardiac hypertrophy and thrombogenesis. Finally, a dual effect of vitamin D was observed in the immune system where it stimulates the innate immune system while tapering down excessive activation of the acquired immune system. Taken together, the vitamin D endocrine system not only regulates calcium homeostasis but affects several systems mainly by altering gene expression but also by ligand-independent actions. SN - 1521-690X UR - https://www.unboundmedicine.com/medline/citation/17161336/Vitamin_D_resistance_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1521-690X(06)00079-0 DB - PRIME DP - Unbound Medicine ER -