IL-18 Production from the NLRP1 Inflammasome Prevents Obesity and Metabolic Syndrome.
Cell Metab
; 23(1): 155-64, 2016 Jan 12.
Article
en En
| MEDLINE
| ID: mdl-26603191
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.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Interleucina-18
/
Síndrome Metabólico
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Proteínas Adaptadoras Transductoras de Señales
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Proteínas Reguladoras de la Apoptosis
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Inflamasomas
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Obesidad
Tipo de estudio:
Etiology_studies
Límite:
Animals
Idioma:
En
Revista:
Cell Metab
Asunto de la revista:
METABOLISMO
Año:
2016
Tipo del documento:
Article
País de afiliación:
Australia