Evidence map›Paper›PMID 27247565›Full record

ReviewGastroenterology research and practice2016

The Pathogenesis of Nonalcoholic Fatty Liver Disease: Interplay between Diet, Gut Microbiota, and Genetic Background.

Jinsheng Yu, Sharon Marsh, Junbo Hu, Wenke Feng, Chaodong Wu

Open access · goldAbstract readReview
In one paragraph

Review in Gastroenterology research and practice, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 4 pooled it
13.8field-weighted citation impact, top 1% 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

101 citing papers in PubMed, 4 syntheses or guidelines pooled it, 197 citations in OpenAlex.

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41 more citing papers are in PubMed but not listed here.

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

5 authors at 5 institutions in 3 countries.

Jinsheng YuDepartment of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA.ORCID 0000-0003-3377-4304
Sharon MarshFaculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, AB, Canada T6G 2H7.
Junbo HuDepartment of General Surgery, Tongji Hospital, Huazhong Science & Technology University, Wuhan, Hubei 430030, China.
Wenke FengDepartment of Medicine, University of Louisville, Louisville, KY 40208, USA.
Chaodong WuDepartment of Nutrition and Food Science, Texas A&M University, Houston, TX 77843, USA.ORCID 0000-0001-8569-8070
Texas A&M University · USTongji Hospital · CNUniversity of Alberta · CAUniversity of Louisville · USWashington University in St. Louis · US

Funding

Protective role of adenosine 2A receptor in NAFLDR01DK095862 · NIDDK · TEXAS A&M AGRILIFE RESEARCH · PI WU, CHAODONG · 2013 to 2017
$1.6M
FGF21 and adipose lipolysis in alcoholic fatty liverR21AA022416 · NIAAA · UNIVERSITY OF LOUISVILLE · PI FENG, WENKE · 2014 to 2015
$388k
NIAAA NIH HHS R21 AA022416NIDDK NIH HHS R01 DK095862
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the world, and it comprises a spectrum of hepatic abnormalities from simple hepatic steatosis to steatohepatitis, fibrosis, cirrhosis, and liver cancer. While the pathogenesis of NAFLD remains incompletely understood, a multihit model has been proposed that accommodates causal factors from a variety of sources, including intestinal and adipose proinflammatory stimuli acting on the liver simultaneously. Prior cellular and molecular studies of patient and animal models have characterized several common pathogenic mechanisms of NAFLD, including proinflammation cytokines, lipotoxicity, oxidative stress, and endoplasmic reticulum stress. In recent years, gut microbiota has gained much attention, and dysbiosis is recognized as a crucial factor in NAFLD. Moreover, several genetic variants have been identified through genome-wide association studies, particularly rs738409 (Ile748Met) in PNPLA3 and rs58542926 (Glu167Lys) in TM6SF2, which are critical risk alleles of the disease. Although a high-fat diet and inactive lifestyles are typical risk factors for NAFLD, the interplay between diet, gut microbiota, and genetic background is believed to be more important in the development and progression of NAFLD. This review summarizes the common pathogenic mechanisms, the gut microbiota relevant mechanisms, and the major genetic variants leading to NAFLD and its progression.

Identifiers

PMID27247565
PMCPMC4876215
OpenAlexW2345961722

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.