Evidence map›Paper›PMID 26678309›Full record

ArticleBMC gastroenterology2015

Deficiency of eNOS exacerbates early-stage NAFLD pathogenesis by changing the fat distribution.

Yuichi Nozaki, Koji Fujita, Koichiro Wada, Masato Yoneda, Yoshiyasu Shinohara, Kento Imajo, Yuji Ogawa, Takaomi Kessoku, Makoto Nakamuta, Satoru Saito and 4 more

Open access · goldAbstract read
In one paragraph

Article in BMC gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.8field-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

25 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
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  10. Chronic liver diseases and erectile dysfunction.Frontiers in public health · 2022
    Review
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  14. Discordant pathological diagnosis of non-alcoholic fatty liver disease: A prospective multicenter study.JGH open : an open access journal of gastroenterology and hepatology · 2020
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. eNOS deletion impairs mitochondrial quality control and exacerbates Western diet-induced NASH.American journal of physiology. Endocrinology and metabolism · 2019
    Article
  20. 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

14 authors at 4 institutions in 1 country.

Yuichi NozakiDepartment of Gastroenterology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, 236-0004, Yokohama, Kanagawa, Japan. fwix0777@nifty.com.
Koji FujitaDepartment of Gastroenterology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, 236-0004, Yokohama, Kanagawa, Japan. kfujita0819@gmail.com.
Koichiro WadaDepartment of Pharmacology, Graduate School of Dentistry, Osaka University, 1-8 Yamadaoka, 565-0871, Suita, Osaka, Japan. kwada@dent.osaka-u.ac.jp.
Masato YonedaDepartment of Gastroenterology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, 236-0004, Yokohama, Kanagawa, Japan. dryoneda@yahoo.co.jp.
Yoshiyasu ShinoharaDepartment of Gastroenterology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, 236-0004, Yokohama, Kanagawa, Japan. shino@hyo-med.ac.jp.
Kento ImajoDepartment of Gastroenterology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, 236-0004, Yokohama, Kanagawa, Japan. kento318@yokohama-cu.ac.jp.
Yuji OgawaDepartment of Gastroenterology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, 236-0004, Yokohama, Kanagawa, Japan. yuji.ogawa01@gmail.com.
Takaomi KessokuDepartment of Gastroenterology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, 236-0004, Yokohama, Kanagawa, Japan. takaomi-kesso@hotmail.co.jp.
Makoto NakamutaDepartment of Gastroenterology, Kyushu Medical Center, National Hospital Organization, 1-8-1, Jigyohama, Chuo-ku, 810-8563, Fukuoka, Japan. nakamuta@kyumed.jp.
Satoru SaitoDepartment of Gastroenterology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, 236-0004, Yokohama, Kanagawa, Japan. ssai1423@yokohama-cu.ac.jp.
Naohiko MasakiThe Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, 1-7-1, Konodai, 272-8516, Ichikawa, China, Japan. nmasaki@hospk.ncgm.go.jp.
Yoji NagashimaDepartment of Molecular Pathology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, 236-0004, Yokohama, Kanagawa, Japan. ynagas@med.yokohama-cu.ac.jp.
Yasuo TerauchiDepartment of Endocrinology and Metabolism, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, 236-0004, Yokohama, Kanagawa, Japan. terauchi-tky@umin.ac.jp.
Atsushi NakajimaDepartment of Gastroenterology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, 236-0004, Yokohama, Kanagawa, Japan. nakajima-tky@umin.ac.jp.
Yokohama City University · JPNational Center for Global Health and Medicine · JPNational Kyushu Medical Center · JPOsaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough many factors and molecules that are closely associated with non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) have been reported, the role of endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) in the pathogenesis of NAFLD/NASH remains unclear. We therefore investigated the role of eNOS-derived NO in NAFLD pathogenesis using systemic eNOS-knockout mice fed a high-fat diet.

methodseNOS-knockout and wild-type mice were fed a basal diet or a high-fat diet for 12 weeks. Lipid accumulation and inflammation were evaluated in the liver, and various factors that are closely associated with NAFLD/NASH and hepatic tissue blood flow were analyzed.

resultsLipid accumulation and inflammation were more extensive in the liver and lipid accumulation was less extensive in the visceral fat tissue in eNOS-knockout mice, compared with wild-type mice, after 12 weeks of being fed a high-fat diet. While systemic insulin resistance was comparable between the eNOS-knockout and wild-type mice fed a high-fat diet, hepatic tissue blood flow was significantly suppressed in the eNOS-knockout mice, compared with the wild-type mice, in mice fed a high-fat diet. The microsomal triglyceride transfer protein activity was down-regulated in eNOS-knockout mice, compared with wild-type mice, in mice fed a high-fat diet.

conclusionsA deficiency of eNOS-derived NO may exacerbate the early-stage of NASH pathogenesis by changing the fat distribution in a mouse model via the regulation of hepatic tissue blood flow.

Indexed as

Lipid MetabolismAnimalsCarrier ProteinsDiet, High-FatInsulin ResistanceLiverMiceMice, KnockoutNitric Oxide Synthase Type IIINon-alcoholic Fatty Liver DiseaseCarrier Proteinsmicrosomal triglyceride transfer proteinNitric Oxide Synthase Type IIINos3 protein, mouse

Identifiers

PMID26678309
PMCPMC4683865
OpenAlexW2200364090

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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.