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The central role of vitamin D in the maintenance of calcium homeostasis is to increase the absorption of ingested calcium from the intestine. The critical importance of vitamin D in this process is noted in the causal link between vitamin D deficiency and rickets, as well as in studies using genetically modified mice including mice deficient in the vitamin D receptor (\n                    <jats:italic>Vdr<\/jats:italic>\n                    null mice) or in the cytochrome P\u2010450 enzyme, 25\u2010hydroxyvitamin D\n                    <jats:sub>3<\/jats:sub>\n                    \u20101\u03b1\u2010 hydroxylase (CYP27B1) that converts 25\u2010hydroxyvitamin D\n                    <jats:sub>3<\/jats:sub>\n                    to the hormonally active form of vitamin D, 1,25\u2010dihydroxyvitamin D\n                    <jats:sub>3<\/jats:sub>\n                    [1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D\n                    <jats:sub>3<\/jats:sub>\n                    ] (\n                    <jats:italic>Cyp27b1<\/jats:italic>\n                    null mice). When these mice are fed diets with high calcium and lactose, rickets is prevented. The studies using mouse models provide supporting evidence indicating that the major physiological function of 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D\n                    <jats:sub>3<\/jats:sub>\n                    \/VDR is intestinal calcium absorption. This review summarizes what is known about mechanisms involved in vitamin D\u2010regulated intestinal calcium absorption. Recent studies suggest that vitamin D does not affect a single entity, but that a complex network of calcium\u2010regulating components is involved in the process of 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D\n                    <jats:sub>3<\/jats:sub>\n                    \u2010mediated active intestinal calcium absorption. In addition, numerous 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D\n                    <jats:sub>3<\/jats:sub>\n                    actions in the intestine have been described independent of calcium absorption. Although the translatability to humans requires further definition, an overview is presented that provides compelling evidence from the laboratory of 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D\n                    <jats:sub>3<\/jats:sub>\n                    intestinal effects, which include the regulation of adhesion molecules to enhance barrier function, the regulation of intestinal stem cell function, cellular homeostasis of other divalent cations, the regulation of drug metabolizing enzymes, and anti\u2010inflammatory effects. \u00a9 2021 The Author.\n                    <jats:italic>JBMR Plus<\/jats:italic>\n                    published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.\n                  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