Evidence map›Paper›PMID 26818807›Full record

ArticleScientific reports2016

Involvement of resistin-like molecule β in the development of methionine-choline deficient diet-induced non-alcoholic steatohepatitis in mice.

Hirofumi Okubo, Akifumi Kushiyama, Hideyuki Sakoda, Yusuke Nakatsu, Masaki Iizuka, Naoyuki Taki, Midori Fujishiro, Toshiaki Fukushima, Hideaki Kamata, Akiko Nagamachi and 8 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. 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
3.1field-weighted citation impact, top 9% 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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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

18 authors at 7 institutions in 1 country.

Hirofumi OkuboDepartment of Medical Science, Graduate School of Medicine, University of Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima Japan.
Akifumi KushiyamaInstitute for Adult Disease, Asahi Life Foundation, 2-2-6, Bakuro-cho, Chuo-ku, Tokyo 103-0002, Japan.
Hideyuki SakodaDepartment of Internal Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo.
Yusuke NakatsuDepartment of Medical Science, Graduate School of Medicine, University of Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima Japan.
Masaki IizukaDepartment of Molecular and Cellular Biology, Kobe Pharma Research Institute, Nippon Boehringer-Ingelheim Co. Ltd. 6-7-5, Minatoshimaminami-cho, Chuo-ku, Kobe city, Hyogo 650-0047, Japan.
Naoyuki TakiDepartment of Molecular and Cellular Biology, Kobe Pharma Research Institute, Nippon Boehringer-Ingelheim Co. Ltd. 6-7-5, Minatoshimaminami-cho, Chuo-ku, Kobe city, Hyogo 650-0047, Japan.
Midori FujishiroDepartment of Internal Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo.
Toshiaki FukushimaDepartment of Medical Science, Graduate School of Medicine, University of Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima Japan.
Hideaki KamataDepartment of Medical Science, Graduate School of Medicine, University of Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima Japan.
Akiko NagamachiDepartment of Molecular Oncology and Leukemia Program Project, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima 734-8553, Japan.
Toshiya InabaDepartment of Molecular Oncology and Leukemia Program Project, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima 734-8553, Japan.
Fusanori NishimuraDepartment of Dental Science for Health Promotion, Division of Cervico-Gnathostomatology, Graduate School of Biomedical Sciences, Hiroshima University, 2-1 Seiryo-machi, Aoba-ku, Sendai, Japan.
Hideki KatagiriDivision of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai, Japan.
Takashi AsaharaYakult Central Institute, Yakult Honsha Co., Ltd. 5-11, Izumi, Kunitachi-shi, 186-8650 Tokyo, Japan.
Yasuto YoshidaYakult Central Institute, Yakult Honsha Co., Ltd. 5-11, Izumi, Kunitachi-shi, 186-8650 Tokyo, Japan.
Osamu ChonanYakult Central Institute, Yakult Honsha Co., Ltd. 5-11, Izumi, Kunitachi-shi, 186-8650 Tokyo, Japan.
Jeffery EncinasDepartment of Molecular and Cellular Biology, Kobe Pharma Research Institute, Nippon Boehringer-Ingelheim Co. Ltd. 6-7-5, Minatoshimaminami-cho, Chuo-ku, Kobe city, Hyogo 650-0047, Japan.
Tomoichiro AsanoDepartment of Medical Science, Graduate School of Medicine, University of Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima Japan.
Hiroshima University · JPBoehringer Ingelheim (Japan) · JPThe University of Tokyo · JPYakult Central Institute · JPInstitute for Adult Diseases Asahi Life Foundation · JPTohoku University · JPYakult Honsha (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resistin-like molecule β (RELMβ) reportedly has multiple functions including local immune responses in the gut. In this study, we investigated the possible contribution of RELMβ to non-alcoholic steatohepatitis (NASH) development. First, RELMβ knock-out (KO) mice were shown to be resistant to methionine-choline deficient (MCD) diet-induced NASH development. Since it was newly revealed that Kupffer cells in the liver express RELMβ and that RELMβ expression levels in the colon and the numbers of RELMβ-positive Kupffer cells were both increased in this model, we carried out further experiments using radiation chimeras between wild-type and RELMβ-KO mice to distinguish between the contributions of RELMβ in these two organs. These experiments revealed the requirement of RELMβ in both organs for full manifestation of NASH, while deletion of each one alone attenuated the development of NASH with reduced serum lipopolysaccharide (LPS) levels. The higher proportion of lactic acid bacteria in the gut microbiota of RELMβ-KO than in that of wild-type mice may be one of the mechanisms underlying the lower serum LPS level the former. These data suggest the contribution of increases in RELMβ in the gut and Kupffer cells to NASH development, raising the possibility of RELMβ being a novel therapeutic target for NASH.

Indexed as

Choline DeficiencyDietAnimalsBiomarkersColonDisease Models, AnimalGastrointestinal MicrobiomeGene Expression RegulationHormones, EctopicIntercellular Signaling Peptides and ProteinsKupffer CellsLiverMacrophagesMaleMethionineMiceBiomarkersHormones, EctopicIntercellular Signaling Peptides and ProteinsMethionineRetnlb protein, mouseToll-Like Receptor 4

Identifiers

PMID26818807
PMCPMC4730188
OpenAlexW2416890568

What OpenQuestion holds

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Registered trials

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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.