Evidence map›Paper›PMID 29408694›Full record

ReviewJournal of hepatology2018

Fructose and sugar: A major mediator of non-alcoholic fatty liver disease.

Thomas Jensen, Manal F Abdelmalek, Shelby Sullivan, Kristen J Nadeau, Melanie Green, Carlos Roncal, Takahiko Nakagawa, Masanari Kuwabara, Yuka Sato, Duk-Hee Kang and 6 more

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Journal of hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04898621 (The Effect of Dietary Fructose on Gut Microbiota and Hepatosteatosis in Healthy Men), which is not on this map. Cited by 460 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
460citing papers in PubMed, 4 pooled it
55.0field-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.

NCT04898621 nacompletednot on this mapstarted 2021, after this paper: background citation

The Effect of Dietary Fructose on Gut Microbiota and Hepatosteatosis in Healthy Men

TypeinterventionalSponsorShanghai Zhongshan HospitalRan2021 to 2022Enrolled58ConditionsHepatic Steatosis, Dietary Fructose ExposureArms75g fructose solution, 150g fructose solution
3 · Its place in the literature

Who cites it

460 citing papers in PubMed, 4 syntheses or guidelines pooled it, 897 citations in OpenAlex.

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400 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

16 authors at 6 institutions in 4 countries.

Thomas JensenDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. Electronic address: Thomas.Jensen@ucdenver.edu.
Manal F AbdelmalekDuke University, Durham, NC, United States.
Shelby SullivanDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Kristen J NadeauDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Melanie GreenDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Carlos RoncalDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Takahiko NakagawaDivision of Future Basic Medicine, Nara Medical University, Nara, Japan.
Masanari KuwabaraDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Yuka SatoDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Duk-Hee KangDivision of Nephrology, Department of Internal Medicine, Ewha Womans University College of Medicine, Seoul, Republic of Korea.
Dean R TolanDept of Biology, Boston University, Boston, MA, United States.
Laura G Sanchez-LozadaLaboratory of Renal Physiopathology, INC Ignacio Chávez, Mexico City, Mexico.
Hugo R RosenDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Miguel A LanaspaDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Anna Mae DiehlDuke University, Durham, NC, United States.
Richard J JohnsonDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
University of Colorado Anschutz Medical Campus · USDuke University · USBoston University · USEwha Womans University · KRInstituto Nacional de Cardiología · MXNara Medical University · JP

Funding

PILOT STUDY--SUBSTRATE METABOLISM IN EXTREMELY LOW BIRTH WEIGHT INFANTSP30DK048520 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Edward L Melanson · 1995 to 2026
$32.6M
Targeting fructokinase, endogenous fructose production and purine degradation for the prevention and treatment of hereditary fructose intoleranceR01DK108859 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Miguel Angel Lanaspa Garcia · 2016 to 2026
$2.4M
Impact of Fructose on Metabolism, Energy Homeostasis and MR biomarkers in NAFLDR01DK093568 · NIDDK · DUKE UNIVERSITY · PI ABDELMALEK, MANAL F., SOHER, BRIAN J · 2012 to 2014
$914k
NIDDK NIH HHS P30 DK048520NIDDK NIH HHS R01 DK093568NIDDK NIH HHS R01 DK108859
6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome; its rising prevalence parallels the rise in obesity and diabetes. Historically thought to result from overnutrition and a sedentary lifestyle, recent evidence suggests that diets high in sugar (from sucrose and/or high-fructose corn syrup [HFCS]) not only increase the risk of NAFLD, but also non-alcoholic steatohepatitis (NASH). Herein, we review the experimental and clinical evidence that fructose precipitates fat accumulation in the liver, due to both increased lipogenesis and impaired fat oxidation. Recent evidence suggests that the predisposition to fatty liver is linked to the metabolism of fructose by fructokinase C, which results in ATP consumption, nucleotide turnover and uric acid generation that mediate fat accumulation. Alterations to gut permeability, the microbiome, and associated endotoxemia contribute to the risk of NAFLD and NASH. Early clinical studies suggest that reducing sugary beverages and total fructose intake, especially from added sugars, may have a significant benefit on reducing hepatic fat accumulation. We suggest larger, more definitive trials to determine if lowering sugar/HFCS intake, and/or blocking uric acid generation, may help reduce NAFLD and its downstream complications of cirrhosis and chronic liver disease.

Indexed as

AnimalsBeveragesCarbonated BeveragesEatingFructokinasesFructoseGastrointestinal MicrobiomeGlucoseHigh Fructose Corn SyrupHumansLipid MetabolismLipogenesisNon-alcoholic Fatty Liver DiseaseOxidation-ReductionRisk FactorsSugarsfructokinaseFructokinasesFructoseGlucoseHigh Fructose Corn SyrupSugarsUric AcidHepatic inflammationHepatic steatosisInsulin resistanceSugar consumptionUric acid

Identifiers

PMID29408694
PMCPMC5893377
OpenAlexW2788821298

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.