Evidence map›Paper›PMID 26487451›Full record

ArticleEuropean journal of nutrition2017

Effects of chronic sugar consumption on lipid accumulation and autophagy in the skeletal muscle.

Daniela De Stefanis, Raffaella Mastrocola, Debora Nigro, Paola Costelli, Manuela Aragno

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Article in European journal of nutrition, 2017. 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
2.7field-weighted citation impact, top 9% 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, 31 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

5 authors at 2 institutions in 1 country.

Daniela De StefanisDepartment of Clinical and Biological Sciences, University of Turin, Corso Raffaello 30, 10125, Turin, Italy.
Raffaella MastrocolaDepartment of Clinical and Biological Sciences, University of Turin, Corso Raffaello 30, 10125, Turin, Italy. raffaella.mastrocola@unito.it.ORCID http://orcid.org/0000-0002-0104-6129
Debora NigroDepartment of Clinical and Biological Sciences, University of Turin, Corso Raffaello 30, 10125, Turin, Italy.
Paola CostelliDepartment of Clinical and Biological Sciences, University of Turin, Corso Raffaello 30, 10125, Turin, Italy.
Manuela AragnoDepartment of Clinical and Biological Sciences, University of Turin, Corso Raffaello 30, 10125, Turin, Italy.
University of Turin · ITSan Raffaele University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeIn recent years, the increasing consumption of soft drinks containing high-fructose corn syrup or sucrose has caused a rise in fructose intake, which has been related to the epidemic of metabolic diseases. As fructose and glucose intake varies in parallel, it is still unclear what the effects of the increased consumption of the two single sugars are. In the present study, the impact of chronic consumption of glucose or fructose on skeletal muscle of healthy mice was investigated.

methodsC57BL/6J male mice received water (C), 15 % fructose (ChF) or 15 % glucose (ChG) to drink for up to 7 months. Lipid metabolism and markers of inflammation and autophagy were assessed in gastrocnemius muscle.

resultsIncreased body weight and gastrocnemius muscle mass, as well as circulating glucose, insulin, and lipid plasma levels were observed in sugar-drinking mice. Although triglycerides increased in the gastrocnemius muscle of both ChF and ChG mice (+32 and +26 %, vs C, respectively), intramyocellular lipids accumulated to a significantly greater extent in ChF than in ChG animals (ChF +10 % vs ChG). Such perturbations were associated with increased muscle interleukin-6 levels (threefold of C) and with the activation of autophagy, as demonstrated by the overexpression of LC3B-II (ChF, threefold and ChG, twofold of C) and beclin-1 (ChF, sevenfold and ChG, tenfold of C).

conclusionsThe present results suggest that intramyocellular lipids and the pro-inflammatory signaling could contribute to the onset of insulin resistance and lead to the induction of autophagy, which could be an adaptive response to lipotoxicity.

Indexed as

AutophagyAnimalsBeclin-1Blood GlucoseCholesterolDisease Models, AnimalFibrinogenFructoseGlucoseInsulinInsulin ResistanceInterleukin-6Lipid MetabolismMaleMetabolic DiseasesMiceBeclin-1Blood GlucoseCholesterolFibrinogenFructoseGlucoseInsulinInterleukin-6Map1lc3b protein, mouseMicrotubule-Associated ProteinsSocs3 protein, mouseSuppressor of Cytokine Signaling 3 ProteinTriglyceridesAutophagyFructoseGlucoseIntramyocellular lipids

Identifiers

PMID26487451
OpenAlexW2178098844

What OpenQuestion holds

Textmetadata
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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.