The endocrine vitamin D system in the gut

The active vitamin D metabolite 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) has important regulatory actions in the gut through endocrine and probably also intracrine, autocrine and paracrine mechanisms. By activating the vitamin D receptor (VDR), which is expressed at a high level in the small intestin...

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Published inMolecular and cellular endocrinology Vol. 453; pp. 79 - 87
Main Authors Barbáchano, Antonio, Fernández-Barral, Asunción, Ferrer-Mayorga, Gemma, Costales-Carrera, Alba, Larriba, María Jesús, Muñoz, Alberto
Format Journal Article
LanguageEnglish
Published Ireland Elsevier B.V 15.09.2017
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Summary:The active vitamin D metabolite 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) has important regulatory actions in the gut through endocrine and probably also intracrine, autocrine and paracrine mechanisms. By activating the vitamin D receptor (VDR), which is expressed at a high level in the small intestine and colon, 1,25(OH)2D3 regulates numerous genes that control gut physiology and homeostasis. 1,25(OH)2D3 is a major responsible for epithelial barrier function and calcium and phosphate absorption, and the host's defense against pathogens and the inflammatory response by several types of secretory and immune cells. Moreover, recent data suggest that 1,25(OH)2D3 has a regulatory effect on the gut microbiota and stromal fibroblasts. Many studies have linked vitamin D deficiency to inflammatory bowel diseases (ulcerative colitis and Crohn's disease) and to an increased risk of colorectal cancer, and the possible use of VDR agonists to prevent or treat these diseases is receiving increasing interest. •Gut expresses a high level of vitamin D receptor and is a main target of vitamin D.•Vitamin D is a major responsible for intestinal Ca2+ and phosphate absorption.•Vitamin D induces gut epithelial barrier function and defense against pathogens.•Vitamin D deficiency is linked to inflammatory bowel diseases.•Vitamin D deficiency is linked to an increased risk of colorectal cancer.
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ISSN:0303-7207
1872-8057
1872-8057
DOI:10.1016/j.mce.2016.11.028