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Title 

Reduced oxidative capacity in macrophages results in systemic insulin resistance

Authors 

S B JungM J ChoiD RyuH S YiS E LeeJ Y ChangH K ChungY K KimS G KangJ H LeeK S KimH J KimC S KimChul Ho LeeR W WilliamsH KimH K LeeJ AuwerxM Shong

Publisher 

Nature Publishing Group

Issue Date 

2018

Citation 

Nature Communications

Abstract 

Oxidative functions of adipose tissue macrophages control the polarization of M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function causes systemic insulin resistance in vivo is not clear. Here, we show that mice with reduced mitochondrial oxidative phosphorylation (OxPhos) due to myeloid-specific deletion of CR6-interacting factor 1 (Crif1), an essential mitoribosomal factor involved in biogenesis of OxPhos subunits, have M1-like polarization of macrophages and systemic insulin resistance with adipose inflammation. Macrophage GDF15 expression is reduced in mice with impaired oxidative function, but induced upon stimulation with rosiglitazone and IL-4. GDF15 upregulates the oxidative function of macrophages, leading to M2-like polarization, and reverses insulin resistance in ob/ob mice and HFD-fed mice with myeloid-specific deletion of Crif1. Thus, reduced macrophage oxidative function controls systemic insulin resistance and adipose inflammation, which can be reversed with GDF15 and leads to improved oxidative function of macrophages

ISSN 

2041-1723

Link 

http://dx.doi.org/10.1038/s41467-018-03998-z

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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