Deletion of Class A Scavenger Receptor Deteriorates Obesity-Induced Insulin Resistance in Adipose Tissue

被引:24
作者
Zhu, Xudong [1 ]
Zong, Guijuan [1 ]
Zhu, Liu [1 ]
Jiang, Yuchen [1 ]
Ma, Ke [1 ]
Zhang, Hanwen [1 ]
Zhang, Yan [1 ]
Bai, Hui [1 ]
Yang, Qing [1 ]
Ben, Jingjing [1 ]
Li, Xiaoyu [1 ]
Xu, Yong [1 ]
Chen, Qi [1 ]
机构
[1] Nanjing Med Univ, Atherosclerosis Res Ctr, Collaborat Innovat Ctr Cardiovasc Dis Translat Me, Key Lab Cardiovasc Dis & Mol Intervent, Nanjing, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
LOW-DENSITY-LIPOPROTEIN; TOLL-LIKE RECEPTORS; MACROPHAGE POLARIZATION; ALTERNATIVE ACTIVATION; METABOLIC DISEASE; LIPID UPTAKE; MICE; LYSOPHOSPHATIDYLCHOLINE; PROTEIN; INFLAMMATION;
D O I
10.2337/db13-0815
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Chronic low-grade inflammation, particularly in the adipose tissue, orchestrates obesity-induced insulin resistance. In this process, polarized activation of macrophages plays a crucial role. However, how macrophages contribute to insulin resistance remains obscure. Class A scavenger receptor (SR-A) is a pattern recognition receptor primarily expressed in macrophages. Through a combination of in vivo and in vitro studies, we report here that deletion of SR-A resulted in reduced insulin sensitivity in obese mice. The anti-inflammatory virtue of SR-A was accomplished by favoring M2 macrophage polarization in adipose tissue. Moreover, we demonstrate that lysophosphatidylcholine (LPC) served as an obesity-related endogenous ligand for SR-A promoting M2 macrophage polarization by activation of signal transducer and activator of transcription 6 signaling. These data have unraveled a clear mechanistic link between insulin resistance and inflammation mediated by the LPC/SR-A pathway in macrophages.
引用
收藏
页码:562 / 577
页数:16
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