Document Detail


Inflammasome is a central player in the induction of obesity and insulin resistance.
MedLine Citation:
PMID:  21876127     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Inflammation plays a key role in the pathogenesis of obesity. Chronic overfeeding leads to macrophage infiltration in the adipose tissue, resulting in proinflammatory cytokine production. Both microbial and endogenous danger signals trigger assembly of the intracellular innate immune sensor Nlrp3, resulting in caspase-1 activation and production of proinflammatory cytokines IL-1β and IL-18. Here, we showed that mice deficient in Nlrp3, apoptosis-associated speck-like protein, and caspase-1 were resistant to the development of high-fat diet-induced obesity, which correlated with protection from obesity-induced insulin resistance. Furthermore, hepatic triglyceride content, adipocyte size, and macrophage infiltration in adipose tissue were all reduced in mice deficient in inflammasome components. Monocyte chemoattractant protein (MCP)-1 is a key molecule that mediates macrophage infiltration. Indeed, defective inflammasome activation was associated with reduced MCP-1 production in adipose tissue. Furthermore, plasma leptin and resistin that affect energy use and insulin sensitivity were also changed by inflammasome-deficiency. Detailed metabolic and molecular phenotyping demonstrated that the inflammasome controls energy expenditure and adipogenic gene expression during chronic overfeeding. These findings reveal a critical function of the inflammasome in obesity and insulin resistance, and suggest inhibition of the inflammasome as a potential therapeutic strategy.
Authors:
Rinke Stienstra; Janna A van Diepen; Cees J Tack; Md Hasan Zaki; Frank L van de Veerdonk; Deshani Perera; Geoffrey A Neale; Guido J Hooiveld; Anneke Hijmans; Irene Vroegrijk; Sjoerd van den Berg; Johannes Romijn; Patrick C N Rensen; Leo A B Joosten; Mihai G Netea; Thirumala-Devi Kanneganti
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-08-29
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  108     ISSN:  1091-6490     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-09-14     Completed Date:  2011-11-09     Revised Date:  2012-03-13    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  15324-9     Citation Subset:  IM    
Affiliation:
Department of Medicine, Radboud University Nijmegen Medical Centre, and Nijmegen Institute for Infection, Inflammation and Immunity, 6525 GA Nijmegen, The Netherlands.
Data Bank Information
Bank Name/Acc. No.:
GEO/GSE25205
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MeSH Terms
Descriptor/Qualifier:
Adipocytes / drug effects,  metabolism,  pathology
Adipose Tissue / pathology
Animals
Carrier Proteins / metabolism
Caspase 1 / metabolism
Cell Movement / drug effects
Cholesterol / blood
Cytoskeletal Proteins / deficiency,  metabolism
Dietary Fats / administration & dosage,  pharmacology
Energy Metabolism / drug effects
Fatty Liver / complications,  pathology,  prevention & control
Glucose Clamp Technique
Humans
Hyperinsulinism / complications,  pathology
Hypertrophy
Inflammasomes / metabolism*
Insulin Resistance*
Macrophages / drug effects,  pathology
Male
Mice
Obesity / blood,  complications,  metabolism*
Triglycerides / blood
Grant Support
ID/Acronym/Agency:
AI088177/AI/NIAID NIH HHS; AR056296/AR/NIAMS NIH HHS
Chemical
Reg. No./Substance:
0/CIAS1 protein, mouse; 0/Carrier Proteins; 0/Cytoskeletal Proteins; 0/Dietary Fats; 0/Inflammasomes; 0/Pycard protein, mouse; 0/Triglycerides; 57-88-5/Cholesterol; EC 3.4.22.36/Caspase 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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