Evidence map›Paper›PMID 24022321›Full record

ArticleNature communications2013

Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome.

Miguel A Lanaspa, Takuji Ishimoto, Nanxing Li, Christina Cicerchi, David J Orlicky, Philip Ruzycki, Philip Ruzicky, Christopher Rivard, Shinichiro Inaba, Carlos A Roncal-Jimenez and 11 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 148 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed, 2 pooled it
8.4field-weighted citation impact, top 2% 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

148 citing papers in PubMed, 2 syntheses or guidelines pooled it, 237 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
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  7. Article
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  10. Article
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    Article
  18. Review
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88 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 5 institutions in 4 countries.

Miguel A Lanaspa1] Division of Renal Diseases and Hypertension, University of Colorado, 12700 East 19th Avenue, Room 7015, Denver, Colorado 80045, USA [2].
Takuji Ishimoto
Nanxing Li
Christina Cicerchi
David J Orlicky
Philip Ruzycki
Philip Ruzicky
Christopher Rivard
Shinichiro Inaba
Carlos A Roncal-Jimenez
Elise S Bales
Christine P Diggle
Aruna Asipu
J Mark Petrash
Tomoki Kosugi
Shoichi Maruyama
Laura G Sanchez-Lozada
James L McManaman
David T Bonthron
Yuri Y Sautin
Richard J Johnson
University of Colorado Denver · USUniversity of Leeds · GBInstituto Nacional de Cardiología · MXNagoya University · JPUniversity of Florida · US

Funding

The functional role of microRNAs in the normal mammary glandP01HD038129 · NICHD · UNIVERSITY OF COLORADO DENVER · PI ANDERSON, STEVEN M · 2000 to 2015
$15.2M
MOLECULAR BIOLOGY OF ALDOSE REDUCTASE AND CATARACTR01EY005856 · NEI · WASHINGTON UNIVERSITY · PI PETRASH, JONATHAN MARK · 1988 to 2014
$6.8M
Role of Uric Acid in Hypertension and Renal DiseaseR01HL068607 · NHLBI · UNIVERSITY OF FLORIDA · PI JOHNSON, RICHARD JOSEPH · 2002 to 2011
$3.5M
Development of inhibitors of AMP Deaminase Isoform 2 as a Mechanism for TreatingRC4DK090859 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI JOHNSON, RICHARD JOSEPH · 2010 to 2010
$2.3M
A novel role for endogenous fructose in ischemic acute kidney injuryK01DK095930 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI LANASPA GARCIA, MIGUEL ANGEL · 2012 to 2016
$686k
NEI NIH HHS R01 EY005856NHLBI NIH HHS HL-68607NHLBI NIH HHS R01 HL068607NICHD NIH HHS P01 HD038129NIDDK NIH HHS 1K01DK095930-01NIDDK NIH HHS K01 DK095930NIDDK NIH HHS RC4 DK090859NIDDK NIH HHS RC4 DK090859-01ORD VA RD04/0002833
6 · The paper itself

Abstract

Carbohydrates with high glycaemic index are proposed to promote the development of obesity, insulin resistance and fatty liver, but the mechanism by which this occurs remains unknown. High serum glucose concentrations are known to induce the polyol pathway and increase fructose generation in the liver. Here we show that this hepatic, endogenously produced fructose causes systemic metabolic changes. We demonstrate that mice unable to metabolize fructose are protected from an increase in energy intake and body weight, visceral obesity, fatty liver, elevated insulin levels and hyperleptinaemia after exposure to 10% glucose for 14 weeks. In normal mice, glucose consumption is accompanied by aldose reductase and polyol pathway activation in steatotic areas. In this regard, we show that aldose reductase-deficient mice are protected against glucose-induced fatty liver. We conclude that endogenous fructose generation and metabolism in the liver represents an important mechanism by which glucose promotes the development of metabolic syndrome.

Indexed as

Aldehyde ReductaseAnimalsEnergy MetabolismFatty LiverFeeding BehaviorFructokinasesFructoseGlucoseHep G2 CellsHumansLiverMetabolic SyndromeMiceMice, Inbred C57BLMice, KnockoutPolymersAldehyde ReductasefructokinaseFructokinasesFructoseGlucosePolymerspolyol

Identifiers

PMID24022321
PMCPMC3833672
OpenAlexW2170672009

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.