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Diabetes. 2014 Feb;63(2):562-77. doi: 10.2337/db13-0815. Epub 2013 Oct 29.

Deletion of class A scavenger receptor deteriorates obesity-induced insulin resistance in adipose tissue.

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Atherosclerosis Research Center, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, China.


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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