IL-37 protects against obesity-induced inflammation and insulin resistance

Ballak, Dov B., Van Diepen, Janna A., Moschen, Alexander R., Jansen, Henry J., Hijmans, Anneke, Groenhof, Gert-jan, Leenders, Floris, Bufler, Philip, Boekschoten, Mark V., Müller, Michael ORCID: https://orcid.org/0000-0002-5930-9905, Kersten, Sander, Li, Suzhao, Kim, Soohyun, Eini, Hadar, Lewis, Eli C., Joosten, Leo A. B., Tilg, Herbert, Netea, Mihai G., Tack, Cees J., Dinarello, Charles A. and Stienstra, Rinke (2014) IL-37 protects against obesity-induced inflammation and insulin resistance. Nature Communications, 5. ISSN 2041-1723

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Abstract

Cytokines of the IL-1 family are important modulators of obesity-induced inflammation and the development of systemic insulin resistance. Here we show that IL-1 family member ​IL-37, recently characterized as an anti-inflammatory cytokine, ameliorates obesity-induced inflammation and insulin resistance. Mice transgenic for human ​IL-37 (​IL-37tg) exhibit reduced numbers of adipose tissue macrophages, increased circulating levels of ​adiponectin and preserved ​glucose tolerance and insulin sensitivity after 16 weeks of HFD. In vitro treatment of adipocytes with recombinant ​IL-37 reduces adipogenesis and activates AMPK signalling. In humans, elevated steady-state ​IL-37 adipose tissue mRNA levels are positively correlated with insulin sensitivity and a lower inflammatory status of the adipose tissue. These findings reveal ​IL-37 as an important anti-inflammatory modulator during obesity-induced inflammation and insulin resistance in both mice and humans, and suggest that ​IL-37 is a potential target for the treatment of obesity-induced insulin resistance and type 2 diabetes.

Item Type: Article
Uncontrolled Keywords: sdg 3 - good health and well-being ,/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being
Faculty \ School: Faculty of Medicine and Health Sciences > Norwich Medical School
Depositing User: Pure Connector
Date Deposited: 08 Oct 2014 08:46
Last Modified: 20 Oct 2022 20:33
URI: https://ueaeprints.uea.ac.uk/id/eprint/50453
DOI: 10.1038/ncomms5711

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