Evidence map›Paper›PMID 36834927›Full record

ArticleInternational journal of molecular sciences2023

Vitamin D Receptor Mediates Attenuating Effect of Lithocholic Acid on Dextran Sulfate Sodium Induced Colitis in Mice.

Hitomi Kubota, Michiyasu Ishizawa, Makoto Kodama, Yoshihiro Nagase, Shigeaki Kato, Makoto Makishima, Kenichi Sakurai

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
6.6field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 26 citations in OpenAlex.

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  3. Vitamin DBiomolecules · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Hitomi KubotaDivision of Biochemistry, Department of Biomedical Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan.
Michiyasu IshizawaDivision of Biochemistry, Department of Biomedical Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan.
Makoto KodamaDepartment of Pathology, Tokyo Yamate Medical Center, 3-22-1 Hyakunin-cho, Shinjuku-ku, Tokyo 169-0073, Japan.
Yoshihiro NagaseDepartment of Pathology, Tokyo Yamate Medical Center, 3-22-1 Hyakunin-cho, Shinjuku-ku, Tokyo 169-0073, Japan.
Shigeaki KatoGraduate School of Science and Technology, Iryo Sosei University, 5-5-1 Iino, Chuodai, Iwaki, Fukushima 970-8044, Japan.
Makoto MakishimaDivision of Biochemistry, Department of Biomedical Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan.ORCID 0000-0002-4630-905X
Kenichi SakuraiDepartment of Surgery, The Nippon Dental University School of Life Dentistry, 2-3-16 Fujimi, Chiyoda-ku, Tokyo 102-8158, Japan.
Nihon University · JPTokyo Yamate Medical Center · JPIRYO Sosei University · JPNippon Dental University · JP

Funding

Japan Society for the Promotion of Science KAKENHI grant number JP16K08632
6 · The paper itself

Abstract

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.

Indexed as

ColitisLithocholic AcidReceptors, CalcitriolAnimalsBile Acids and SaltsDextran SulfateMiceMice, Inbred C57BLBile Acids and SaltsDextran SulfateLithocholic AcidReceptors, Calcitriolbile aciddextran sulfate sodiumhypercalcemiainflammatory bowel diseaseintestinal mucosal injurylithocholic acidvitamin D receptor

Identifiers

PMID36834927
PMCPMC9965401
OpenAlexW4319985547

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.