Evidence map›Paper›PMID 27111539›Full record

Trial reportPloS one2016

Skeletal Muscle Insulin Resistance and Absence of Inflammation Characterize Insulin-Resistant Grade I Obese Women.

Cacylde Amouzou, Cyril Breuker, Odile Fabre, Annick Bourret, Karen Lambert, Olivier Birot, Christine Fédou, Anne-Marie Dupuy, Jean-Paul Cristol, Thibault Sutra and 9 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.1field-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

22 citing papers in PubMed, 33 citations in OpenAlex.

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  14. Metabolically healthy obesity: facts and fantasies.The Journal of clinical investigation · 2019
    Review
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  18. Expression of macrophage genes within skeletal muscle correlates inversely with adiposity and insulin resistance in humans.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2018
    Article
  19. Article
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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

19 authors at 6 institutions in 2 countries.

Cacylde AmouzouPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Cyril BreukerPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Odile FabrePhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Annick BourretPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Karen LambertPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Olivier BirotFaculty of Health, York University, York, Ontario, Canada.
Christine FédouPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Anne-Marie DupuyCentre Hospitalier Régional Universitaire (CHRU) Montpellier, Montpellier, France.
Jean-Paul CristolPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Thibault SutraPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Nicolas MolinariPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Laurent MaimounPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Denis Mariano-GoulartPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Florence GaltierCentre Hospitalier Régional Universitaire (CHRU) Montpellier, Montpellier, France.
Antoine AvignonPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Françoise Stanke-LabesqueUniversity of Grenoble Alpes, INSERM U1042, HP2, Grenoble, CHU Albert Michalon, Grenoble, France.
Jacques MercierPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Ariane SultanPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Catherine BisbalPhyMedExp, University of Montpellier, INSERM U1046, CNRS UMR 9214, Montpellier, France.
Physiologie et Médecine Expérimentale du Coeur et des Muscles · FRCentre Hospitalier Universitaire de Montpellier · FRInserm · FRUniversité de Montpellier · FRCentre National de la Recherche Scientifique · FRYork University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextObesity is associated with insulin-resistance (IR), the key feature of type 2 diabetes. Although chronic low-grade inflammation has been identified as a central effector of IR development, it has never been investigated simultaneously at systemic level and locally in skeletal muscle and adipose tissue in obese humans characterized for their insulin sensitivity.

objectivesWe compared metabolic parameters and inflammation at systemic and tissue levels in normal-weight and obese subjects with different insulin sensitivity to better understand the mechanisms involved in IR development.

methods30 post-menopausal women were classified as normal-weight insulin-sensitive (controls, CT) and obese (grade I) insulin-sensitive (OIS) or insulin-resistant (OIR) according to their body mass index and homeostasis model assessment of IR index. They underwent a hyperinsulinemic-euglycemic clamp, blood sampling, skeletal muscle and subcutaneous adipose tissue biopsies, an activity questionnaire and a self-administrated dietary recall. We analyzed insulin sensitivity, inflammation and IR-related parameters at the systemic level. In tissues, insulin response was assessed by P-Akt/Akt expression and inflammation by macrophage infiltration as well as cytokines and IκBα expression.

resultsSystemic levels of lipids, adipokines, inflammatory cytokines, and lipopolysaccharides were equivalent between OIS and OIR subjects. In subcutaneous adipose tissue, the number of anti-inflammatory macrophages was higher in OIR than in CT and OIS and was associated with higher IL-6 level. Insulin induced Akt phosphorylation to the same extent in CT, OIS and OIR. In skeletal muscle, we could not detect any inflammation even though IκBα expression was lower in OIR compared to CT. However, while P-Akt/Akt level increased following insulin stimulation in CT and OIS, it remained unchanged in OIR.

conclusionOur results show that systemic IR occurs without any change in systemic and tissues inflammation. We identified a muscle defect in insulin response as an early mechanism of IR development in grade I obese post-menopausal women.

Indexed as

Insulin ResistanceBlood GlucoseCase-Control StudiesCell MovementC-Reactive ProteinDiabetes Mellitus, Type 2DietFemaleGene Expression RegulationGlucose Clamp TechniqueHumansInflammationInsulinInterleukin-6LipopolysaccharidesMacrophagesBlood GlucoseC-Reactive ProteinIL6 protein, humanInsulinInterleukin-6LipopolysaccharidesNF-KappaB Inhibitor alphaProto-Oncogene Proteins c-akt

Identifiers

PMID27111539
PMCPMC4844150
OpenAlexW2344838470

What OpenQuestion holds

Textmetadata
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.