Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
The Journal of Experimental Medicine
Year: 2010  |  Volume: 206  |  Issue: 13  |  Page No.: 3143 - 3156

MGL1 promotes adipose tissue inflammation and insulin resistance by regulating 7/4hi monocytes in obesity

D. J Westcott, J. B DelProposto, L. M Geletka, T Wang, K Singer, A. R Saltiel and C. N. Lumeng    

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.

View Fulltext    |   Related Articles   |   Back
   
 
 
 
  Related Articles

No Article Found
 
 
 
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility