The Inflammasome Puts Obesity in the Danger Zone

被引：228

作者：

Stienstra, Rinke ^{[1
,2
,3
]}

Tack, Cees J. ^{[1
]}

Kanneganti, Thirumala-Devi ^{[4
]}

Joosten, Leo A. B. ^{[1
,2
]}

Netea, Mihai G. ^{[1
,2
]}

机构：

[1] Radboud Univ Nijmegen, Med Ctr, Dept Med, NL-6525 GA Nijmegen, Netherlands

[2] Radboud Univ Nijmegen, Med Ctr, Nijmegen Inst Infect Inflammat & Immun N4I, NL-6525 GA Nijmegen, Netherlands

[3] Wageningen Univ, Nutr Metab & Genom Grp, NL-6703 HD Wageningen, Netherlands

[4] St Jude Childrens Res Hosp, Dept Immunol, Memphis, TN 38105 USA

来源：

CELL METABOLISM | 2012年 / 15卷 / 01期

关键词：

THIOREDOXIN-INTERACTING PROTEIN; ISLET AMYLOID POLYPEPTIDE; SATURATED FATTY-ACIDS; INSULIN-RESISTANCE; CASPASE-1; ACTIVATION; NLRP3; INFLAMMASOME; ADIPOSE-TISSUE; DOUBLE-BLIND; RECEPTOR; URIC-ACID;

D O I：

10.1016/j.cmet.2011.10.011

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Obesity-induced inflammation is an important contributor to the induction of insulin resistance. Recently, the cytokine interleukin-1 beta (IL-1 beta) has emerged as a prominent instigator of the proinflammatory response in obesity. Several studies over the last year have subsequently deciphered the molecular mechanisms responsible for IL-1 beta activation in adipose tissue, liver, and macrophages and demonstrated a central role of the processing enzyme caspase-1 and of the protein complex leading to its activation called the inflammasome. These data suggest that activation of the inflammasome represents a crucial step in the road from obesity to insulin resistance and type 2 diabetes.

引用

收藏

页码：10 / 18

页数：9

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