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

  1. Qi Chen
  1. Atherosclerosis Research Center, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, China
  1. Corresponding author: Qi Chen, qichen{at}njmu.edu.cn.

Abstract

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.

Footnotes

  • Received May 22, 2013.
  • Accepted October 22, 2013.

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  1. Diabetes vol. 63 no. 2 562-577
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