Abstract
Biotin deficiency is often overlooked in patients with Inflammatory Bowel Disease, but it may have profound implications in the GI tract. Biotin is a water-soluble vitamin that must be obtained from exogenous sources and is involved in the metabolism of fatty acids, glucose and amino acids. Recently, we have studied the impact of biotin deficiency, induced by dietary or genetic methods, in mice and have found that they develop growth retardation, decreased bone density, and histological changes in intestine that are similar to what we find in patients with IBD. Importantly, these mice fully recover with biotin supplementation. We have found that intestinal tight junction (TJ) proteins, which are necessary for maintaining mucosal integrity, are downregulated when the host is biotin deficient and this “leaky gut” induces colitis. TJ expression returns to baseline when biotin is supplemented and we questioned whether biotin could be used as a therapeutic in other models for colitis. We treated mice with 3% DSS in drinking water to induce colitis and after seven days they had significant weight loss, increased disease activity index, increased fecal calprotectin, decreased colon length, increased pro-inflammatory cytokines and worse intestinal histologic scores, as expected. In addition, they also had decreased levels of the biotin transporter (SMVT), decreased tight TJ proteins (ZO-1 and Occludin), increased leaky TJ protein (claudin-1) and increased gut permeability. If these mice had 1mM biotin supplemented to their drinking water, then all parameters returned towards baseline. These data suggest that biotin supplementation may be able to treat or prevent colitis in patients with Inflammatory Bowel Disease. Biotin is available over the counter, is affordable and has minimal side effect profile making it an ideal therapeutic if clinical trials can show the same efficacy as we have seen in this pre-clinical model. This project is supported by: VA CDA 5IK2BX003518, NIH (TR001415, DK58057, DK56061, and AA018071)
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