Role of interleukins in obesity: implications for metabolic disease

被引:102
作者
Febbraio, Mark A. [1 ]
机构
[1] Baker IDI Heart & Diabet Inst, Cellular & Mol Metab Lab, Melbourne, Vic, Australia
基金
英国医学研究理事会; 澳大利亚研究理事会;
关键词
interleukins; inflammasome; beta cell; nutrient overload; INDUCED INSULIN-RESISTANCE; TYPE-2; DIABETES-MELLITUS; ACTIVATED PROTEIN-KINASE; NECROSIS-FACTOR-ALPHA; SKELETAL-MUSCLE AMPK; NF-KAPPA-B; GLUCOSE-HOMEOSTASIS; PLASMA INTERLEUKIN-6; NLRP3; INFLAMMASOME; CARBOHYDRATE-METABOLISM;
D O I
10.1016/j.tem.2014.02.004
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
It has been two decades since the discovery that pro-inflammatory cytokines are expressed in obesity. This initial work was the catalyst for the now-accepted paradigm that nutrient overload promotes inflammation and links the metabolic and immune systems, where inflammation may be pathological. However, inflammation is an adaptive and, importantly, an energy-consuming process. Indeed, the rapid mobilization of stored energy reserves by cytokines such as the interleukins, is critical to mounting any successful inflammatory response. Thus, the role of the interleukins in metabolism and energy homeostasis is more complex than first thought and recent evidence is mounting that, for several interleukins, although excess production is negative, blockade or insufficiency is equally undesirable.
引用
收藏
页码:312 / 319
页数:8
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