MGL1 promotes adipose tissue inflammation and insulin resistance by regulating 7/4hi monocytes in obesity
Open Access
- 7 December 2009
- journal article
- Published by Rockefeller University Press in The Journal of Experimental Medicine
- Vol. 206 (13), 3143-3156
- https://doi.org/10.1084/jem.20091333
Abstract
Adipose tissue macrophages (ATMs) play a critical role in obesity-induced inflammation and insulin resistance. Distinct subtypes of ATMs have been identified that differentially express macrophage galactose-type C-type lectin 1 (MGL1/CD301), a marker of alternatively activated macrophages. To evaluate if MGL1 is required for the anti-inflammatory function of resident (type 2) MGL1+ ATMs, we examined the effects of diet-induced obesity (DIO) on inflammation and metabolism in Mgl1−/− mice. We found that Mgl1 is not required for the trafficking of type 2 ATMs to adipose tissue. Surprisingly, obese Mgl1−/− mice were protected from glucose intolerance, insulin resistance, and steatosis despite having more visceral fat. This protection was caused by a significant decrease in inflammatory (type 1) CD11c+ ATMs in the visceral adipose tissue of Mgl1−/− mice. MGL1 was expressed specifically in 7/4hi inflammatory monocytes in the blood and obese Mgl1−/− mice had lower levels of 7/4hi monocytes. Mgl1−/− monocytes had decreased half-life after adoptive transfer and demonstrated decreased adhesion to adipocytes indicating a role for MGL1 in the regulation of monocyte function. This study identifies MGL1 as a novel regulator of inflammatory monocyte trafficking to adipose tissue in response to DIO.Keywords
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