Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

    We have a manual that explains all the features 

Record number 530668
Title The inflammasome is a central player in the induction of obesity and insulin resistance
Author(s) Stienstra, Rinke; Diepen, Janna A. van; Tack, Cees J.; Zaki, Mohammad H.; Veerdonk, Frank L. van de; Perera, Deshani; Neal, Geoff; Hijmans, Anneke; Vroegrijk, Irene O.; Berg, Sjoerd A. van den; Romijn, Johannes A.; Rensen, Patrick C.; Joosten, Leo A.; Netea, Mihai G.; Kanneganti, Thirumala-Devi D.
Department(s) Chair Nutrition Metabolism and Genomics
Publication type Dataset
Publication year 2011
Keyword(s) GSE25205 - Mus musculus - PRJNA134319
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.
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