RBP4 activates antigen-presenting cells, leading to adipose tissue inflammation and systemic insulin resistance.

ABSTRACT: Insulin resistance is a major cause of diabetes and is highly associated with adipose tissue (AT) inflammation in obesity. RBP4, a retinol transporter, is elevated in insulin resistance and contributes to increased diabetes risk. We aimed to determine the mechanisms for RBP4-induced insulin resistance. Here we show that RBP4 elevation causes AT inflammation by activating innate immunity that elicits an adaptive immune response. RBP4-overexpressing mice (RBP4-Ox) are insulin resistant and glucose intolerant and have increased AT macrophage and CD4 T cell infiltration. In RBP4-Ox, AT CD206(+) macrophages express proinflammatory markers and activate CD4 T cells while maintaining alternatively activated macrophage markers. These effects result from direct activation of AT antigen-presenting ce

SUBMITTER: Moraes-Vieira PM 

PROVIDER: S-EPMC4078000 | biostudies-literature | 2014 Mar

REPOSITORIES: biostudies-literature