Evidence map›Paper›PMID 27295340›Full record

ArticleScientific reports2016

Ecophysiological consequences of alcoholism on human gut microbiota: implications for ethanol-related pathogenesis of colon cancer.

Atsuki Tsuruya, Akika Kuwahara, Yuta Saito, Haruhiko Yamaguchi, Takahisa Tsubo, Shogo Suga, Makoto Inai, Yuichi Aoki, Seiji Takahashi, Eri Tsutsumi and 11 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 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

58 citing papers in PubMed, 101 citations in OpenAlex.

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  16. Gut Microbiome Interactions with Oxidative Stress: Mechanisms and Consequences for Health.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024
    Review
  17. Article
  18. The Past and Future of Inflammation as a Target to Cancer Prevention.Cancer prevention research (Philadelphia, Pa.) · 2024
    Article
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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

21 authors at 6 institutions in 1 country.

Atsuki TsuruyaDepartment of Biomolecular Engineering, Graduate School of Engineering, Tohoku University, Sendai, Miyagi 980-8579 Japan.
Akika KuwaharaDepartment of Biomolecular Engineering, Graduate School of Engineering, Tohoku University, Sendai, Miyagi 980-8579 Japan.
Yuta SaitoDepartment of Biomolecular Engineering, Graduate School of Engineering, Tohoku University, Sendai, Miyagi 980-8579 Japan.
Haruhiko YamaguchiDepartment of Biomolecular Engineering, Graduate School of Engineering, Tohoku University, Sendai, Miyagi 980-8579 Japan.
Takahisa TsuboDepartment of Biomolecular Engineering, Graduate School of Engineering, Tohoku University, Sendai, Miyagi 980-8579 Japan.
Shogo SugaDepartment of Biomolecular Engineering, Graduate School of Engineering, Tohoku University, Sendai, Miyagi 980-8579 Japan.
Makoto InaiDepartment of Biomolecular Engineering, Graduate School of Engineering, Tohoku University, Sendai, Miyagi 980-8579 Japan.
Yuichi AokiDepartment of Applied Information Sciences, Graduate School of Information Sciences, Tohoku University, Sendai, Miyagi 980-8579 Japan.
Seiji TakahashiDepartment of Biomolecular Engineering, Graduate School of Engineering, Tohoku University, Sendai, Miyagi 980-8579 Japan.
Eri TsutsumiSuntory World Research Center, Suntory Holdings Ltd., Soraku-gun, Kyoto 619-0284, Japan.
Yoshihide SuwaSuntory World Research Center, Suntory Holdings Ltd., Soraku-gun, Kyoto 619-0284, Japan.
Hidetoshi MoritaGraduate School of Environmental and Life Science, Okayama University, 1-1-1 Tsushima-naka, Kita-ku, Okayama 700-8530, Japan.
Kenji KinoshitaSchool of Pharmaceutical Sciences, Mukogawa Women's University, Nishinomiya, Hyogo 663-8179, Japan.
Yukari TotsukaDivision of Cancer Development System, National Cancer Center Research Institute, Chuo-ku, Tokyo 104-0045, Japan.
Wataru SudaCenter for Omics and Bioinformatics, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Chiba 277-8561, Japan.
Kenshiro OshimaCenter for Omics and Bioinformatics, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Chiba 277-8561, Japan.
Masahira HattoriCenter for Omics and Bioinformatics, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Chiba 277-8561, Japan.
Takeshi MizukamiNational Hospital Organization Kurihama Medical and Addiction Center, Yokosuka, Kanagawa 239-0841, Japan.
Akira YokoyamaNational Hospital Organization Kurihama Medical and Addiction Center, Yokosuka, Kanagawa 239-0841, Japan.
Takefumi ShimoyamaDepartment of Biomolecular Engineering, Graduate School of Engineering, Tohoku University, Sendai, Miyagi 980-8579 Japan.
Toru NakayamaDepartment of Biomolecular Engineering, Graduate School of Engineering, Tohoku University, Sendai, Miyagi 980-8579 Japan.
Tohoku University · JPThe University of Tokyo · JPKurihama Medical and Addiction Center · JPSuntory (Japan) · JPMukogawa Women's University · JPOkayama University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic consumption of excess ethanol increases the risk of colorectal cancer. The pathogenesis of ethanol-related colorectal cancer (ER-CRC) is thought to be partly mediated by gut microbes. Specifically, bacteria in the colon and rectum convert ethanol to acetaldehyde (AcH), which is carcinogenic. However, the effects of chronic ethanol consumption on the human gut microbiome are poorly understood, and the role of gut microbes in the proposed AcH-mediated pathogenesis of ER-CRC remains to be elaborated. Here we analyse and compare the gut microbiota structures of non-alcoholics and alcoholics. The gut microbiotas of alcoholics were diminished in dominant obligate anaerobes (e.g., Bacteroides and Ruminococcus) and enriched in Streptococcus and other minor species. This alteration might be exacerbated by habitual smoking. These observations could at least partly be explained by the susceptibility of obligate anaerobes to reactive oxygen species, which are increased by chronic exposure of the gut mucosa to ethanol. The AcH productivity from ethanol was much lower in the faeces of alcoholic patients than in faeces of non-alcoholic subjects. The faecal phenotype of the alcoholics could be rationalised based on their gut microbiota structures and the ability of gut bacteria to accumulate AcH from ethanol.

Indexed as

Gastrointestinal MicrobiomeAcetaldehydeAdolescentAdultAgedAlcohol DehydrogenaseAlcoholismAldehyde Dehydrogenase, MitochondrialBacteroidesCluster AnalysisColorectal NeoplasmsEthanolFecesFemaleHumansMaleAcetaldehydeADH1B protein, humanAlcohol DehydrogenaseAldehyde Dehydrogenase, MitochondrialALDH2 protein, humanEthanolRNA, Ribosomal, 16S

Identifiers

PMID27295340
PMCPMC4904738
OpenAlexW2439965773

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.