{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T23:34:52Z","timestamp":1791588892665,"version":"4.3.4"},"reference-count":54,"publisher":"MDPI AG","issue":"4","license":[{"start":{"date-parts":[[2023,2,9]],"date-time":"2023-02-09T00:00:00Z","timestamp":1675900800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"JSPS KAKENHI","award":["JP16K08632"],"award-info":[{"award-number":["JP16K08632"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Bile acids are major components of bile; they emulsify dietary lipids for efficient digestion and absorption and act as signaling molecules that activate nuclear and membrane receptors. The vitamin D receptor (VDR) is a receptor for the active form of vitamin D and lithocholic acid (LCA), a secondary bile acid produced by the intestinal microflora. Unlike other bile acids that enter the enterohepatic circulation, LCA is poorly absorbed in the intestine. Although vitamin D signaling regulates various physiological functions, including calcium metabolism and inflammation\/immunity, LCA signaling remains largely unknown. In this study, we investigated the effect of the oral administration of LCA on colitis in a mouse model using dextran sulfate sodium (DSS). Oral LCA decreased the disease activity of colitis in the early phase, which is a phenotype associated with the suppression of histological injury, such as inflammatory cell infiltration and goblet cell loss. These protective effects of LCA were abolished in VDR-deleted mice. LCA decreased the expression of inflammatory cytokine genes, but this effect was at least partly observed in VDR-deleted mice. The pharmacological effect of LCA on colitis was not associated with hypercalcemia, an adverse effect induced by vitamin D compounds. Therefore, LCA suppresses DSS-induced intestinal injury in its action as a VDR ligand.<\/jats:p>","DOI":"10.3390\/ijms24043517","type":"journal-article","created":{"date-parts":[[2023,2,10]],"date-time":"2023-02-10T02:56:13Z","timestamp":1675997773000},"page":"3517","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Vitamin D Receptor Mediates Attenuating Effect of Lithocholic Acid on Dextran Sulfate Sodium Induced Colitis in Mice"],"prefix":"10.3390","volume":"24","author":[{"given":"Hitomi","family":"Kubota","sequence":"first","affiliation":[{"name":"Division of Biochemistry, Department of Biomedical Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan"},{"name":"Department of Surgery, The Nippon Dental University School of Life Dentistry, 2-3-16 Fujimi, Chiyoda-ku, Tokyo 102-8158, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michiyasu","family":"Ishizawa","sequence":"additional","affiliation":[{"name":"Division of Biochemistry, Department of Biomedical Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Makoto","family":"Kodama","sequence":"additional","affiliation":[{"name":"Department of Pathology, Tokyo Yamate Medical Center, 3-22-1 Hyakunin-cho, Shinjuku-ku, Tokyo 169-0073, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshihiro","family":"Nagase","sequence":"additional","affiliation":[{"name":"Department of Pathology, Tokyo Yamate Medical Center, 3-22-1 Hyakunin-cho, Shinjuku-ku, Tokyo 169-0073, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shigeaki","family":"Kato","sequence":"additional","affiliation":[{"name":"Graduate School of Science and Technology, Iryo Sosei University, 5-5-1 Iino, Chuodai, Iwaki, Fukushima 970-8044, Japan"},{"name":"Research Institute of Innovative Medicine, Tokiwa Foundation, Kaminodai-57 Jobankamiyunagayamachi, Iwaki, Fukushima 972-8322, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4630-905X","authenticated-orcid":false,"given":"Makoto","family":"Makishima","sequence":"additional","affiliation":[{"name":"Division of Biochemistry, Department of Biomedical Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenichi","family":"Sakurai","sequence":"additional","affiliation":[{"name":"Department of Surgery, The Nippon Dental University School of Life Dentistry, 2-3-16 Fujimi, Chiyoda-ku, Tokyo 102-8158, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,2,9]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"bqac155","DOI":"10.1210\/endocr\/bqac155","article-title":"Bile acids\u2014A peek into their history and signaling","volume":"163","author":"Nguyen","year":"2022","journal-title":"Endocrinology"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"S120","DOI":"10.1194\/jlr.R800026-JLR200","article-title":"Fifty years of advances in bile acid synthesis and metabolism","volume":"50","author":"Russell","year":"2009","journal-title":"J. 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