Evidence map›Paper›PMID 29063269›Full record

ArticleJournal of gastroenterology2018

Slow-metabolizing ADH1B and inactive heterozygous ALDH2 increase vulnerability to fatty liver in Japanese men with alcohol dependence.

Akira Yokoyama, Nobuhito Taniki, Sachiko Hara, Emiko Haysashi, Nobuhiro Nakamoto, Takeshi Mizukami, Katsuya Maruyama, Tetsuji Yokoyama

Abstract read
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In one paragraph

Article in Journal of gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

6 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Role of ALDH2 in Hepatic Disorders: Gene Polymorphism and Disease Pathogenesis.Journal of clinical and translational hepatology · 2021
    Review
  5. Article
  6. Review
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

8 authors at 3 institutions in 1 country.

Akira YokoyamaNational Hospital Organization Kurihama Medical and Addiction Center, 5-3-1 Nobi, Yokosuka, Kanagawa, 239-0841, Japan. a_yokoyama@kurihama1.hosp.go.jp.
Nobuhito TanikiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo, 160-8582, Japan.
Sachiko HaraNational Hospital Organization Kurihama Medical and Addiction Center, 5-3-1 Nobi, Yokosuka, Kanagawa, 239-0841, Japan.
Emiko HaysashiNational Hospital Organization Kurihama Medical and Addiction Center, 5-3-1 Nobi, Yokosuka, Kanagawa, 239-0841, Japan.
Nobuhiro NakamotoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo, 160-8582, Japan.
Takeshi MizukamiNational Hospital Organization Kurihama Medical and Addiction Center, 5-3-1 Nobi, Yokosuka, Kanagawa, 239-0841, Japan.
Katsuya MaruyamaNational Hospital Organization Kurihama Medical and Addiction Center, 5-3-1 Nobi, Yokosuka, Kanagawa, 239-0841, Japan.
Tetsuji YokoyamaDepartment of Health Promotion, National Institute of Public Health, 2-3-6 Minami, Wako, Saitama, 351-0104, Japan.
Kurihama Medical and Addiction Center · JPKeio University · JPNational Institute of Public Health · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenetic polymorphisms of alcohol dehydrogenase-1B (ADH1B; rs1229984, His48Arg) and aldehyde dehydrogenase-2 (ALDH2; rs671, Glu504Lys) affect body weight, body fat, and lipid metabolism in individuals with alcohol dependence, and the aim of this study was to identify their determinants in relation to the development of fatty liver.

methodsWe evaluated associations between the presence of fatty liver and ADH1B and ALDH2 genotypes and other factors in 1604 Japanese men who had been admitted for treatment of alcohol dependence.

resultsFatty liver was diagnosed when ultrasonography showed both hepatorenal contrast and liver brightness. Age-adjusted usual alcohol intake did not differ according to ADH1B or ALDH2 genotypes. A multivariate analysis showed that the adjusted odds ratio (OR, 95% confidence interval) of slow-metabolizing ADH1B Arg/Arg carriers was 1.61 (1.27-2.03) for fatty liver and 1.82 (1.37-2.41) for fatty liver with deep attenuation in comparison with the ADH1B His/Arg or His/His carriers, and that the OR of inactive heterozygous ALDH2 Glu/Lys carriers was 1.43 (1.08-1.91) for fatty liver and 1.84 (1.31-2.59) for fatty liver with deep attenuation in comparison with the ALDH2 Glu/Glu carriers. Younger age, shorter interval between the last drink and the ultrasound examination, larger body mass index, and absence of cirrhosis were identified as other positive determinants for fatty liver.

conclusionsThe ADH1B Arg/Arg genotype and the ALDH2 Glu/Lys genotype were positive determinants of fatty liver in the subjects. These results suggest that slow ethanol and acetaldehyde metabolism accelerates the development of alcoholic fatty liver in heavy drinkers.

Indexed as

AdultAgedAge FactorsAlcohol DehydrogenaseAlcoholismAldehyde Dehydrogenase, MitochondrialBody Mass IndexFatty Liver, AlcoholicHeterozygoteHumansJapanMaleMiddle AgedTime FactorsUltrasonographyADH1B protein, humanAlcohol DehydrogenaseAldehyde Dehydrogenase, MitochondrialALDH2 protein, humanAcetaldehydeAlcohol dehydrogenase-1BAldehyde dehydrogenase-2Body mass indexCirrhosisFatty liver

Identifiers

PMID29063269
OpenAlexW2766406757

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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.