Evidence map›Paper›PMID 27194405›Full record

ArticleScientific reports2016

Fructose, but not glucose, impairs insulin signaling in the three major insulin-sensitive tissues.

Miguel Baena, Gemma Sangüesa, Alberto Dávalos, María-Jesús Latasa, Aleix Sala-Vila, Rosa María Sánchez, Núria Roglans, Juan Carlos Laguna, Marta Alegret

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
8.2field-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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

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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

9 authors at 5 institutions in 1 country.

Miguel BaenaDepartment of Pharmacology and Therapeutic Chemistry, School of Pharmacy, University of Barcelona, Spain.
Gemma SangüesaDepartment of Pharmacology and Therapeutic Chemistry, School of Pharmacy, University of Barcelona, Spain.
Alberto DávalosIMDEA Food. CEI UAM+CSIC, Madrid, Spain.
María-Jesús LatasaIMDEA Food. CEI UAM+CSIC, Madrid, Spain.
Aleix Sala-VilaCIBER Fisiología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Spain.
Rosa María SánchezDepartment of Pharmacology and Therapeutic Chemistry, School of Pharmacy, University of Barcelona, Spain.
Núria RoglansDepartment of Pharmacology and Therapeutic Chemistry, School of Pharmacy, University of Barcelona, Spain.
Juan Carlos LagunaDepartment of Pharmacology and Therapeutic Chemistry, School of Pharmacy, University of Barcelona, Spain.
Marta AlegretDepartment of Pharmacology and Therapeutic Chemistry, School of Pharmacy, University of Barcelona, Spain.
Instituto de Salud Carlos III · ESInstitute for Research in Biomedicine · ESUniversitat de Barcelona · ESIMDEA Food · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human studies support the relationship between high intake of fructose-sweetened beverages and type 2 diabetes, but there is a debate on whether this effect is fructose-specific or it is merely associated to an excessive caloric intake. Here we investigate the effects of 2 months' supplementation to female rats of equicaloric 10% w/v fructose or glucose solutions on insulin sensitivity in target tissues. Fructose supplementation caused hepatic deposition of triglycerides and changed the fatty acid profile of this fraction, with an increase in monounsaturated and a decrease in polyunsaturated species, but did not cause inflammation and oxidative stress. Fructose but not glucose-supplemented rats displayed an abnormal glucose tolerance test, and did not show increased phosphorylation of V-akt murine thymoma viral oncogene homolog-2 (Akt) in white adipose tissue and liver after insulin administration. In skeletal muscle, phosphorylation of Akt and of Akt substrate of 160 kDA (AS160) was not impaired but the expression of the glucose transporter type 4 (GLUT4) in the plasma membrane was reduced only in fructose-fed rats. In conclusion, fructose but not glucose supplementation causes fatty liver without inflammation and oxidative stress and impairs insulin signaling in the three major insulin-responsive tissues independently from the increase in energy intake.

Indexed as

Signal TransductionAdipose TissueAnimalsDietFatty LiverFructoseGlucoseGlucose Tolerance TestHypoglycemic AgentsInsulinLiverMuscle, SkeletalRatsSweetening AgentsFructoseGlucoseHypoglycemic AgentsInsulinSweetening Agents

Identifiers

PMID27194405
PMCPMC4872141
OpenAlexW2399321381

What OpenQuestion holds

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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.