SMILED SIGNED
Skeletal Muscle Inflammation: ambivalent roles in Exercise and Diabetes
Total Cost €
0EC-Contrib. €
0Partnership
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Project "SMILED" data sheet
The following table provides information about the project.
| Coordinator |
KAROLINSKA INSTITUTET
Organization address contact info |
| 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 |
Partnership
Take a look of project's partnership.
| # | ||||
|---|---|---|---|---|
| 1 | KAROLINSKA INSTITUTET | SE (STOCKHOLM) | coordinator | 185˙857.00 |
Map
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.
Publications
| year | authors and title | journal | last update |
|---|---|---|---|
| 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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