Inflammatory Mechanisms in Obesity

被引:2649
作者
Gregor, Margaret F. [1 ]
Hotamisligil, Goekhan S.
机构
[1] Harvard Univ, Sch Publ Hlth, Dept Genet, Boston, MA 02115 USA
来源
ANNUAL REVIEW OF IMMUNOLOGY, VOL 29 | 2011年 / 29卷
关键词
adiposity; metaflammation; insulin resistance; inflammatory signaling; organelle stress; nutrient signals; TUMOR-NECROSIS-FACTOR; INDUCED INSULIN-RESISTANCE; NF-KAPPA-B; DIET-INDUCED OBESITY; ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN RESPONSE; HIGH-FAT DIET; ADIPOSE-TISSUE INFLAMMATION; TYPE-2; DIABETES-MELLITUS; FACTOR-ALPHA BLOCKADE;
D O I
10.1146/annurev-immunol-031210-101322
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The modern rise in obesity and its strong association with insulin resistance and type 2 diabetes have elicited interest in the underlying mechanisms of these pathologies. The discovery that obesity itself results in an inflammatory state in metabolic tissues ushered in a research field that examines the inflammatory mechanisms in obesity. Here, we summarize the unique features of this metabolic inflammatory state, termed metaflammation and defined as low-grade, chronic inflammation orchestrated by metabolic cells in response to excess nutrients and energy. We explore the effects of such inflammation in metabolic tissues including adipose, liver, muscle, pancreas, and brain and its contribution to insulin resistance and metabolic dysfunction. Another area in which many unknowns still exist is the origin or mechanism of initiation of inflammatory signaling in obesity. We discuss signals or triggers to the inflammatory response, including the possibility of endoplasmic reticulum stress as an important contributor to metaflammation. Finally, we examine anti-inflammatory therapies for their potential in the treatment of obesity-related insulin resistance and glucose intolerance.
引用
收藏
页码:415 / 445
页数:31
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