Evidence map›Paper›PMID 31760464›Full record

ReviewCellular and molecular life sciences : CMLS2020

Fructose-mediated effects on gene expression and epigenetic mechanisms associated with NAFLD pathogenesis.

Johanna K DiStefano

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 79 citations in OpenAlex.

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  9. Common Denominator of MASLD and Some Non-Communicable Diseases.Current issues in molecular biology · 2024
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  20. Physiopathology of nonalcoholic fatty liver disease: from diet to nutrigenomics.Current opinion in clinical nutrition and metabolic care · 2022
    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

1 author at 1 institution in 1 country.

Johanna K DiStefanoDiabetes and Fibrotic Disease Unit, Translational Genomics Research Institute, 445 N 5th Street, Phoenix, AZ, 85004, USA. jdistefano@tgen.org.ORCID http://orcid.org/0000-0002-3286-0270
Translational Genomics Research Institute · US

Funding

Epigenetic markers of severity in nonalcoholic fatty liver diseaseR01DK107735 · NIDDK · TRANSLATIONAL GENOMICS RESEARCH INST · PI DISTEFANO, JOHANNA K, GERHARD, GLENN S · 2016 to 2020
$3.1M
NIDDK NIH HHS DK107735NIDDK NIH HHS R01 DK107735
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a chronic, frequently progressive condition that develops in response to excessive hepatocyte fat accumulation (i.e., steatosis) in the absence of significant alcohol consumption. Liver steatosis develops as a result of imbalanced lipid metabolism, driven largely by increased rates of de novo lipogenesis and hepatic fatty acid uptake and reduced fatty acid oxidation and/or disposal to the circulation. Fructose is a naturally occurring simple sugar, which is most commonly consumed in modern diets in the form of sucrose, a disaccharide comprised of one molecule of fructose covalently bonded with one molecule of glucose. A number of observational and experimental studies have demonstrated detrimental effects of dietary fructose consumption not only on diverse metabolic outcomes such as insulin resistance and obesity, but also on hepatic steatosis and NAFLD-related fibrosis. Despite the compelling evidence that excessive fructose consumption is associated with the presence of NAFLD and may even promote the development and progression of NAFLD to more clinically severe phenotypes, the molecular mechanisms by which fructose elicits effects on dysregulated liver metabolism remain unclear. Emerging data suggest that dietary fructose may directly alter the expression of genes involved in lipid metabolism, including those that increase hepatic fat accumulation or reduce hepatic fat removal. The aim of this review is to summarize the current research supporting a role for dietary fructose intake in the modulation of transcriptomic and epigenetic mechanisms underlying the pathogenesis of NAFLD.

Indexed as

Epigenesis, GeneticAnimalsDietary SugarsDisease Models, AnimalDNA MethylationFructoseHumansLipid MetabolismNon-alcoholic Fatty Liver DiseaseTranscriptomeDietary SugarsFructoseAnimal modelsDietDNA methylationEpigenetics, microRNAHepatic steatosisNonalcoholic fatty liver diseaseTranscriptomics

Identifiers

PMID31760464
PMCPMC7440926
OpenAlexW2991474498

What OpenQuestion holds

Textmetadata
LicenceTDM
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.