期刊
JOURNAL OF PARENTERAL AND ENTERAL NUTRITION
卷 32, 期 6, 页码 638-644出版社
WILEY
DOI: 10.1177/0148607108325251
关键词
type 2 diabetes; insulin resistance; adiposity-associated inflammation; adipose tissue; insulin; fatty acids
资金
- NHLBI NIH HHS [P50 HL083799-01, R01 HL-073278, R01 HL073278-01, P50 HL-083799, P50 HL083799, R01 HL073278] Funding Source: Medline
- NIDDK NIH HHS [P30 DK-019525, U13 DK064190, P30 DK019525-27, P30 DK019525, R01 DK-021224] Funding Source: Medline
- RMOD NIH HHS [RFA-RM-06-002] Funding Source: Medline
Adiposity-associated inflammation and insulin resistance are strongly implicated in the development of type 2 diabetes and atherosclerotic cardiovascular disease. This article reviews the mechanisms of adipose inflammation, because these may represent therapeutic targets for insulin resistance and for prevention of metabolic and cardiovascular consequences of obesity. The initial insult in adipose inflammation and insulin resistance, mediated by macrophage recruitment and endogenous ligand activation of Toll-like receptors, is perpetuated through chemokine secretion, adipose retention of macrophages, and elaboration of pro-inflammatory adipocytokines. Activation of various kinases modulates adipocyte transcription factors, including peroxisome proliferator-activated receptor-gamma and NF kappa B, attenuating insulin signaling and increasing adipocytokine and free fatty acid secretion. Inflammation retards adipocyte differentiation and further exacerbates adipose dysfunction and inflammation. Paracrine and endocrine adipose inflammatory events induce a local and systemic inflammatory, insulin-resistant state promoting meta-bolic dyslipidemia, type 2 diabetes, and cardiovascular disease. Developing therapeutic strategies that target both adipose inflammation and insulin resistance may help to prevent type 2 diabetes and cardiovascular disease in the emerging epidemic of obesity. (JPEN J Parenter Enteral Man 2008;32:638-644)
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据