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Skeletal Muscle Inflammation: ambivalent roles in Exercise and Diabetes

Total Cost €


EC-Contrib. €






 SMILED project word cloud

Explore the words cloud of the SMILED project. It provides you a very rough idea of what is the project "SMILED" about.

people    cardiovascular    unmanageable    human    genes    glucose    treatment    fact    profiling    occurs    myopathies    roles    million    expression    diseases    interaction    muscle    surprisingly    links    rnas    therapeutic    potent    skeletal    methylation    anti    abnormal    events    induces    tissue    highlights    homeostasis    strategies    repair    t2d    biopsies    90    signal    exercise    interventional    sensitivity    little    leads    severe    economic    multifactorial    inflammation    parallel    complications    diabetes    lifestyle    metabolism    hallmark    cell    disease    innovative    metabolic    constitutes    ambivalent    environmental    diet    plays    52    living    translate    chromatin    small    burden    promoter    physical    contributor    epigenetic    obesity    suggested    transduction    sedentary    despite    inflammatory    primary    insulin    regulations    intervention    discoveries    unknown    effect    molecular    structure    adipose    proof    greatest    dependent    beneficial    suggesting    obtain    dna    local    cultures   

Project "SMILED" data sheet

The following table provides information about the project.


Organization address
address: Nobels Vag 5
postcode: 17177

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Sweden [SE]
 Total cost 185˙857 €
 EC max contribution 185˙857 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-05-01   to  2018-04-30


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KAROLINSKA INSTITUTET SE (STOCKHOLM) coordinator 185˙857.00


 Project objective

In Europe, 52 million people are living with diabetes, with more than 90% of them having type 2 diabetes (T2D), a multifactorial disease associated with obesity and sedentary lifestyle. It leads to severe complications such as cardiovascular events and constitutes an unmanageable economic burden. Skeletal muscle inflammation is emerging as a potential contributor to T2D. Inflammation occurs during exercise and repair and is a hallmark of myopathies, suggesting that it plays crucial roles in skeletal muscle homeostasis. Despite the fact that exercise is associated with inflammation, physical activity has beneficial effects on T2D, which highlights the ambivalent role of muscle inflammation in controlling glucose homeostasis. Epigenetic processes are potential molecular links between diseases and environmental factors such as diet and exercise. Abnormal promoter methylation of inflammatory genes was recently suggested in adipose tissue during obesity, but little is currently known about epigenetic regulations in muscle during exercise and diabetes. Surprisingly, it is unknown whether there is any parallel between local inflammation of muscle and T2D and no therapeutic strategies currently target skeletal muscle for T2D treatment. The overall aim of this proposal is to determine the interaction between inflammation and the metabolic response to exercise and T2D to define potent interventional strategies that can improve insulin sensitivity. It will identify what type of inflammatory response induces the greatest metabolic effect on signal transduction and expression of genes through profiling DNA methylation, chromatin structure and small RNAs. It will use primary cell cultures from human biopsies to (1) obtain proof of principle that the beneficial effect of exercise on metabolism is dependent on inflammation, and (2) translate these discoveries into innovative exercise and anti-inflammatory intervention strategies to improve insulin sensitivity.


year authors and title journal last update
List of publications.
2017 Nicolas J. Pillon, Anna Krook
Innate immune receptors in skeletal muscle metabolism
published pages: 47-54, ISSN: 0014-4827, DOI: 10.1016/j.yexcr.2017.02.035
Experimental Cell Research 360/1 2019-06-13
2018 Evangelia Daskalaki, Nicolas J. Pillon, Anna Krook, Craig E. Wheelock, Antonio Checa
The influence of culture media upon observed cell secretome metabolite profiles: The balance between cell viability and data interpretability
published pages: , ISSN: 0003-2670, DOI: 10.1016/j.aca.2018.04.034
Analytica Chimica Acta 2019-06-13
2018 Nicolas J Pillon, Scott Frendo-Cumbo, Maya R Jacobson, Zhi Liu, Paul L Milligan, Hai Hoang Bui, Juleen R Zierath, Philip J Bilan, Joseph T Brozinick, Amira Klip
Cell-autonomous sphingolipid changes do not underlie fatty acid-induced insulin resistance of GLUT4 translocation or pro-inflammatory signaling in muscle cells
published pages: jlr.M080788, ISSN: 0022-2275, DOI: 10.1194/jlr.M080788
Journal of Lipid Research 2019-06-13
2018 Christophe O. Soulage, Laura Sardón Puig, Laurent Soulère, Bader Zarrouki, Michel Guichardant, Michel Lagarde, Nicolas J. Pillon
Skeletal muscle insulin resistance is induced by 4-hydroxy-2-hexenal, a by-product of n-3 fatty acid peroxidation
published pages: 688-699, ISSN: 0012-186X, DOI: 10.1007/s00125-017-4528-4
Diabetologia 61/3 2019-06-13

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