IL-18 production from the NLRP1 inflammasome prevents obesity and metabolic syndrome
Details
Publication Year 2016-01-12,Volume 23,Issue #1,Page 155-164
Journal Title
Cell Metabolism
Publication Type
Journal Article
Abstract
Summary Interleukin-18 (IL-18) is activated by Caspase-1 in inflammasome complexes and has anti-obesity effects; however, it is not known which inflammasome regulates this process. We found that mice lacking the NLRP1 inflammasome phenocopy mice lacking IL-18, with spontaneous obesity due to intrinsic lipid accumulation. This is exacerbated when the mice are fed a high-fat diet (HFD) or a high-protein diet, but not when mice are fed a HFD with low energy density (high fiber). Furthermore, mice with an activating mutation in NLRP1, and hence increased IL-18, have decreased adiposity and are resistant to diet-induced metabolic dysfunction. Feeding these mice a HFD further increased plasma IL-18 concentrations and strikingly resulted in loss of adipose tissue mass and fatal cachexia, which could be prevented by genetic deletion of IL-18. Thus, NLRP1 is an innate immune sensor that functions in the context of metabolic stress to produce IL-18, preventing obesity and metabolic syndrome.
Publisher
Cell Press
Research Division(s)
Inflammation; Population Health And Immunity; Systems Biology And Personalised Medicine; Cancer And Haematology; Immunology; Chemical Biology
PubMed ID
26603191
Terms of Use/Rights Notice
Refer to copyright notice on published article.


Creation Date: 2015-11-19 02:00:40
Last Modified: 2019-04-01 08:56:50
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