Evidence map›Paper›PMID 40990870›Full record

ArticleThe International journal of eating disorders2026

DSOK-0011 Potentially Regulates Circadian Misalignment and Affects Gut Microbiota Composition in Activity-Based Anorexia Model.

Hiroki Kawai, Nanami Wada, Shinji Sakamoto, Kenji Miyazaki, Taro Kato, Yoshihiro Horiuchi, Hiroshi Kirii, Hoang Duy Nguyen, Kenji Hinotsu, Yoshio Ohya and 6 more

Abstract read
In one paragraph

Article in The International journal of eating disorders, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

16 authors.

Hiroki KawaiDepartment of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.ORCID https://orcid.org/0000-0002-4441-9896
Nanami WadaDepartment of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Shinji SakamotoDepartment of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.ORCID https://orcid.org/0000-0001-5498-551X
Kenji MiyazakiSumitomo Pharma Co. Ltd, Osaka, Japan.
Taro KatoSumitomo Pharma Co. Ltd, Osaka, Japan.
Yoshihiro HoriuchiSumitomo Pharma Co. Ltd, Osaka, Japan.
Hiroshi KiriiDepartment of Animal Applied Microbiology, Okayama University Graduate School of Environmental, Life, Natural Science and Technology, Okayama, Japan.
Hoang Duy NguyenDepartment of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Kenji HinotsuDepartment of Neuropsychiatry, Okayama University Hospital, Okayama, Japan.
Yoshio OhyaDepartment of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Takahiro AsadaDepartment of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Akiyoshi YokodeDepartment of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Yuko OkahisaDepartment of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Haruko MiyazakiDepartment of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Toshitaka OohashiDepartment of Molecular Biology and Biochemistry, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Manabu TakakiDepartment of Neuropsychiatry, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.

Funding

Japan Society for the Promotion of Science 22K07616Japan Society for the Promotion of Science 23H04235Japan Society for the Promotion of Science 24K10679Japan Society for the Promotion of Science 24K10733Japan Society for the Promotion of Science 24KK0155Japan Society for the Promotion of Science 25K19080Oofuji Endocrine MedicalSumitomo Pharma Co. Ltd.
6 · The paper itself

Abstract

objectiveAnorexia nervosa (AN) is a metabolic-psychiatric disorder characterized by severe weight loss, hypercortisolemia, and hypothalamic-pituitary-adrenal (HPA) axis activation. In this study, we investigated the effect of inhibiting cortisol regeneration via the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) on the pathophysiology of AN.

methodFemale C57BL/6J mice underwent a 7-day activity-based anorexia (ABA) paradigm, involving 3 h daily feeding and free access to wheels, until 25% body weight loss or experiment completion. Mice were orally treated once daily with a potent 11β-HSD1 inhibitor, DSOK-0011, or vehicle. Body weight, food intake, and activity transitions were recorded; plasma corticosterone and cholesterol levels were measured using a fluorometric assay; gut microbiota were analyzed using 16S rRNA sequencing; and hippocampal glial cells were analyzed using immunohistochemistry.

resultsDSOK-0011-treated mice exhibited a modest but significant increase in postprandial wheel-running activity compared to baseline (4-5 p.m., p = 0.018; 5-6 p.m., p = 0.043), whereas vehicle-treated mice showed higher preprandial activity (9-10 a.m., p = 0.0229). Gut microbiota analysis revealed increased alpha diversity in ABA mice, with a specific enrichment of the Lachnospiraceae family in the DSOK-0011 group. However, DSOK-0011 did not significantly affect body weight, food intake, corticosterone, and lipid levels, or hippocampal glial cell populations.

conclusionInhibition of 11β-HSD1 by DSOK-0011 was associated with microbiota alterations and subtle shifts in activity timing under energy-deficient conditions. These findings suggest that peripheral glucocorticoid metabolism may influence microbial and behavioral responses in the ABA model, although its metabolic impact appears limited in the acute phase.

Indexed as

11-beta-Hydroxysteroid Dehydrogenase Type 1AnorexiaAnorexia NervosaCircadian RhythmGastrointestinal MicrobiomeAnimalsCorticosteroneDisease Models, AnimalFemaleMiceMice, Inbred C57BL11-beta-Hydroxysteroid Dehydrogenase Type 1Corticosterone11β‐HSD1activity‐based anorexiaanorexia nervosacorticosteroneeating disordersmicrobiota

Identifiers

PMID40990870
PMCPMC12773686

What OpenQuestion holds

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LicenceCC BY-NC
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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.