Evidence map›Paper›PMID 30469339›Full record

ReviewNutrients2018

Copper-Fructose Interactions: A Novel Mechanism in the Pathogenesis of NAFLD.

Ming Song, Miriam B Vos, Craig J McClain

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  5. Dietary therapy of murine primary biliary cholangitis induces hepatocellular steatosis: A cautionary tale.Liver international : official journal of the International Association for the Study of the Liver · 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

3 authors at 3 institutions in 1 country.

Ming SongDepartment of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Louisville School of Medicine, Louisville, KY 40202, USA. m0song03@louisville.edu.
Miriam B VosDepartment of Pediatrics, Emory University School of Medicine, Atlanta, GA 30307, USA. MVOS@emory.edu.
Craig J McClainDepartment of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Louisville School of Medicine, Louisville, KY 40202, USA. cjmccl01@louisville.edu.
Children's Healthcare of Atlanta · USLouisville VA Medical Center · USUniversity of Louisville · US

Funding

Role of oxidized linoleic acid metabolites in the pathogenesis of alcoholic liver diseaseP20GM113226 · NIGMS · UNIVERSITY OF LOUISVILLE · PI MCCLAIN, CRAIG J. · 2016 to 2025
$24.1M
The Role of Nutrition in the Development/Progression of Alcohol-Induced Organ InjuryP50AA024337 · NIAAA · UNIVERSITY OF LOUISVILLE · PI CRAIG J. MCCLAIN · 2016 to 2026
$17.9M
Tumor Necrosis Factor and Alcoholic Liver DiseaseR37AA010762 · NIAAA · UNIVERSITY OF LOUISVILLE · PI MCCLAIN, CRAIG J. · 2001 to 2010
$3.6M
The Role of Alcohol in HIV Therapy HepatotoxicityR01AA018016 · NIAAA · UNIVERSITY OF LOUISVILLE · PI BARVE, SHIRISH S, EATON, JOHN W · 2008 to 2012
$1.7M
Biomarkers for SteatohepatitisRC2AA019385 · NIAAA · UNIVERSITY OF LOUISVILLE · PI MCCLAIN, CRAIG J. · 2009 to 2010
$1.6M
University of Louisville Bioinformatics Faculty Recruitment for EpigeneticsP30AA019360 · NIAAA · UNIVERSITY OF LOUISVILLE · PI MCCLAIN, CRAIG J. · 2009 to 2010
$811k
Dietary Fat and Alcoholic Liver DiseaseI01BX002996 · VA · LOUISVILLE VA MEDICAL MEDICAL CENTER · PI MCCLAIN, CRAIG J. · 2017 to 2020
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BLRD VA I01 BX002996NIAAA NIH HHS P50 AA024337NIGMS NIH HHS P20 GM113226NIH HHS P20GM113226NIH HHS P30AA019360NIH HHS P50AA024337NIH HHS PO1AA017103NIH HHS R01AA018016NIH HHS R37AA010762NIH HHS RC2AA019385NIH HHS RO1AA015970NIH HHS RO1AA018869NIH HHS RO1DK071765
6 · The paper itself

Abstract

Compelling epidemiologic data support the critical role of dietary fructose in the epidemic of obesity, metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). The metabolic effects of fructose on the development of metabolic syndrome and NAFLD are not completely understood. High fructose intake impairs copper status, and copper-fructose interactions have been well documented in rats. Altered copper-fructose metabolism leads to exacerbated experimental metabolic syndrome and NAFLD. A growing body of evidence has demonstrated that copper levels are low in NAFLD patients. Moreover, hepatic and serum copper levels are inversely correlated with the severity of NAFLD. Thus, high fructose consumption and low copper availability are considered two important risk factors in NAFLD. However, the causal effect of copper-fructose interactions as well as the effects of fructose intake on copper status remain to be evaluated in humans. The aim of this review is to summarize the role of copper-fructose interactions in the pathogenesis of the metabolic syndrome and discuss the potential underlying mechanisms. This review will shed light on the role of copper homeostasis and high fructose intake and point to copper-fructose interactions as novel mechanisms in the fructose induced NAFLD.

Indexed as

AnimalsCopperDisease Models, AnimalFructoseHumansMetabolic SyndromeNon-alcoholic Fatty Liver DiseaseObesityRisk FactorsCopperFructosecopperfructosegut microbiotaironkupffer cell (KC)metabolic syndromenon-alcoholic fatty liver disease (NAFLD)

Identifiers

PMID30469339
PMCPMC6266129
OpenAlexW2897933627

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.