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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.

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

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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