Evidence map›Paper›PMID 23861559›Full record

ArticleMediators of inflammation2013

High sugar intake and development of skeletal muscle insulin resistance and inflammation in mice: a protective role for PPAR- δ agonism.

Elisa Benetti, Raffaella Mastrocola, Mara Rogazzo, Fausto Chiazza, Manuela Aragno, Roberto Fantozzi, Massimo Collino, Marco A Minetto

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  11. International journal of molecular sciences · 2018
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Skeletal muscle inflammation and insulin resistance in obesity.The Journal of clinical investigation · 2017
    Review
  17. Article
  18. Diabetes and dyslipidemia: characterizing lipoprotein metabolism.Diabetes, metabolic syndrome and obesity : targets and therapy · 2017
    Review
  19. Article
  20. Article
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

8 authors at 1 institution in 1 country.

Elisa BenettiDepartment of Drug Science and Technology, University of Turin, Via Giuria 9, 10125 Torino, Italy.
Raffaella Mastrocola
Mara Rogazzo
Fausto Chiazza
Manuela Aragno
Roberto Fantozzi
Massimo Collino
Marco A Minetto
University of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Peroxisome Proliferator Activated Receptor (PPAR)- δ agonists may serve for treating metabolic diseases. However, the effects of PPAR- δ agonism within the skeletal muscle, which plays a key role in whole-body glucose metabolism, remain unclear. This study aimed to investigate the signaling pathways activated in the gastrocnemius muscle by chronic administration of the selective PPAR- δ agonist, GW0742 (1 mg/kg/day for 16 weeks), in male C57Bl6/J mice treated for 30 weeks with high-fructose corn syrup (HFCS), the major sweetener in foods and soft-drinks (15% wt/vol in drinking water). Mice fed with the HFCS diet exhibited hyperlipidemia, hyperinsulinemia, hyperleptinemia, and hypoadiponectinemia. In the gastrocnemius muscle, HFCS impaired insulin and AMP-activated protein kinase signaling pathways and reduced GLUT-4 and GLUT-5 expression and membrane translocation. GW0742 administration induced PPAR- δ upregulation and improvement in glucose and lipid metabolism. Diet-induced activation of nuclear factor-κB and expression of inducible-nitric-oxide-synthase and intercellular-adhesion-molecule-1 were attenuated by drug treatment. These effects were accompanied by reduction in the serum concentration of interleukin-6 and increase in muscular expression of fibroblast growth factor-21. Overall, here we show that PPAR- δ activation protects the skeletal muscle against the metabolic abnormalities caused by chronic HFCS exposure by affecting multiple levels of the insulin and inflammatory cascades.

Indexed as

Gene Expression RegulationInsulin ResistanceAnimalsCarbohydratesFibroblast Growth FactorsGlucoseGlucose Tolerance TestImmunohistochemistryInflammationInsulinInterleukin-6Lipid MetabolismMaleMiceMice, Inbred C57BLMuscle, Skeletal(4-(((2-(3-fluoro-4-(trifluoromethyl)phenyl)-4-methyl-1,3-thiazol-5-yl)methyl)sulfanyl)-2-methylphenoxy)acetic acidCarbohydratesfibroblast growth factor 21Fibroblast Growth FactorsGlucoseInsulinInterleukin-6Nutritive SweetenersPhenolsPPAR deltaSulfhydryl CompoundsThiazoles

Identifiers

PMID23861559
PMCPMC3703883
OpenAlexW2167790121

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.