Deletion of Class A Scavenger Receptor Deteriorates Obesity-Induced Insulin Resistance in Adipose Tissue
Author(s) -
Xudong Zhu,
Guijuan Zong,
Liu Zhu,
Yuchen Jiang,
Ke Ma,
Hanwen Zhang,
Yan Zhang,
Hui Bai,
Qing Yang,
Jingjing Ben,
Xiaoyu Li,
Yong Xu,
Qi Chen
Publication year - 2013
Publication title -
diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.219
H-Index - 330
eISSN - 1939-327X
pISSN - 0012-1797
DOI - 10.2337/db13-0815
Subject(s) - adipose tissue , insulin resistance , scavenger receptor , macrophage polarization , endocrinology , medicine , inflammation , adipose tissue macrophages , receptor , biology , insulin receptor , white adipose tissue , microbiology and biotechnology , activator (genetics) , insulin , macrophage , in vitro , biochemistry , cholesterol , lipoprotein
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.
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