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Review
. 2016 Jan 21;22(3):933-48.
doi: 10.3748/wjg.v22.i3.933.

Protective links between vitamin D, inflammatory bowel disease and colon cancer

Stacey Meeker  1 , Audrey Seamons  1 , Lillian Maggio-Price  1 , Jisun Paik  1
Affiliations
Review

Protective links between vitamin D, inflammatory bowel disease and colon cancer

Stacey Meeker et al. World J Gastroenterol. .

Abstract

Vitamin D deficiency has been associated with a wide range of diseases and multiple forms of cancer including breast, colon, and prostate cancers. Relatively recent work has demonstrated vitamin D to be critical in immune function and therefore important in inflammatory diseases such as inflammatory bowel disease (IBD). Because vitamin D deficiency or insufficiency is increasingly prevalent around the world, with an estimated 30%-50% of children and adults at risk for vitamin D deficiency worldwide, it could have a significant impact on IBD. Epidemiologic studies suggest that low serum vitamin D levels are a risk factor for IBD and colon cancer, and vitamin D supplementation is associated with decreased colitis disease activity and/or alleviated symptoms. Patients diagnosed with IBD have a higher incidence of colorectal cancer than the general population, which supports the notion that inflammation plays a key role in cancer development and underscores the importance of understanding how vitamin D influences inflammation and its cancer-promoting effects. In addition to human epidemiological data, studies utilizing mouse models of colitis have shown that vitamin D is beneficial in preventing or ameliorating inflammation and clinical disease. The precise role of vitamin D on colitis is unknown; however, vitamin D regulates immune cell trafficking and differentiation, gut barrier function and antimicrobial peptide synthesis, all of which may be protective from IBD and colon cancer. Here we focus on effects of vitamin D on inflammation and inflammation-associated colon cancer and discuss the potential use of vitamin D for protection and treatment of IBD and colon cancer.

Keywords: Colitis; Colon cancer; Inflammation-associated colon cancer; Inflammatory bowel disease; Mouse models; Vitamin D.

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Figures

Figure 1
Figure 1
Vitamin D metabolism. Vitamin D can be obtained either through exposure to sunlight where ultraviolet B (UVB) interaction in the skin converts 7-dehydrocholesterol to vitamin D or through absorption from the diet. Vitamin D must undergo several hydroxylation steps to become an active metabolite, 1,25-dihydroxyvitamin D. The first hydroxylation step occurring mainly in liver by 25-hydroxylase produces 25-hydroxyvitamin D, the main circulating form of vitamin D. The second hydroxylation step catalyzed by 1α-hydroxylase occurs in many target tissues including kidney, intestinal epithelial cells and immune cells and generates the active form of vitamin D, 1,25-dihydroxyvitamin D. This latter form of vitamin D is a ligand for a transcription factor, vitamin D receptor (VDR), which is present in most cell types. VDR bound with 1,25-dihydroxyvitamin D translocates to the nucleus where it dimerizes with retinoid X receptor (RXR). The dimers have the ability to activate transcription of various genes containing a specific promoter region known as vitamin D response elements (VDRE) by binding to the region and recruiting transcriptional machinery.
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