Dataset Information


The inflammasome is a central player in the induction of obesity and insulin resistance

ABSTRACT: Inflammation plays a key role in the pathogenesis of obesity. Chronic overfeeding leads to macrophage infiltration in the adipose tissue, resulting in pro-inflammatory cytokine production. Both microbial and endogenous danger signals trigger assembly of the intracellular innate immune sensor Nlrp3 [NLR family, pyrin domain containing 3] resulting in caspase-1 activation and production of pro-inflammatory cytokines interleukin (IL)-1beta and IL-18. Here, we showed that mice deficient in Nlrp3, ASC [apoptosis-associated speck-like protein containing a CARD; a.k.a PYCARD (PYD and CARD domain containing)] and caspase-1 were resistant to the development of high fat diet-induced obesity, which correlated with protection from obesity-induced insulin resistance. 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. Keywords: Expression profiling by array Wild-type (WT), ASC-null and Casp1-null mice were subjected to high fat diet feeding for 16 weeks. After the diet intervention period, the animals were killed and epididymal white adipose tissue was removed. Total RNA was isolated and subjected to gene expression profiling.

ORGANISM(S): Mus musculus  

SUBMITTER: Janna A van Diepen   Geoff Neal  Deshani Perera  Thirumala-Devi D Kanneganti  Sjoerd A van den Berg  Cees J Tack  Frank L van de Veerdonk  Leo A Joosten  Rinke Stienstra  Guido Hooiveld  Johannes A Romijn  Mohammad H Zaki  Irene O Vroegrijk  Patrick C Rensen  Anneke Hijmans  Mihai G Netea 

PROVIDER: E-GEOD-25205 | ArrayExpress | 2011-08-20



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