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RBP4 Activates Antigen-Presenting Cells, Leading to Adipose Tissue Inflammation and Systemic Insulin Resistance

Cell metabolism, 2014-03, Vol.19 (3), p.512-526 [Peer Reviewed Journal]

2014 Elsevier Inc. ;Copyright © 2014 Elsevier Inc. All rights reserved. ;2014 Elsevier Inc. All rights reserved. 2014 ;ISSN: 1550-4131 ;EISSN: 1932-7420 ;DOI: 10.1016/j.cmet.2014.01.018 ;PMID: 24606904

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Title:
RBP4 Activates Antigen-Presenting Cells, Leading to Adipose Tissue Inflammation and Systemic Insulin Resistance
Author: Moraes-Vieira, Pedro M. ; Yore, Mark M. ; Dwyer, Peter M. ; Syed, Ismail ; Aryal, Pratik ; Kahn, Barbara B.
Subjects: Adipose Tissue - cytology ; Adipose Tissue - metabolism ; Animals ; Antigen-Presenting Cells - cytology ; Antigen-Presenting Cells - metabolism ; Bone Marrow Cells - cytology ; CD4-Positive T-Lymphocytes - cytology ; CD4-Positive T-Lymphocytes - immunology ; CD4-Positive T-Lymphocytes - metabolism ; Cell Proliferation ; Glucose Intolerance ; Humans ; Insulin Resistance ; JNK Mitogen-Activated Protein Kinases - metabolism ; Lectins, C-Type - metabolism ; Liver - cytology ; Macrophages - cytology ; Macrophages - drug effects ; Macrophages - metabolism ; Male ; Mannose-Binding Lectins - metabolism ; Mice ; Mice, Inbred C57BL ; Receptors, Cell Surface - metabolism ; Recombinant Proteins - biosynthesis ; Recombinant Proteins - genetics ; Recombinant Proteins - pharmacology ; Retinol-Binding Proteins, Plasma - genetics ; Retinol-Binding Proteins, Plasma - metabolism ; Retinol-Binding Proteins, Plasma - pharmacology ; Signal Transduction ; Th1 Cells - cytology ; Th1 Cells - metabolism ; Transcriptome
Is Part Of: Cell metabolism, 2014-03, Vol.19 (3), p.512-526
Description: 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 cells (APCs) by RBP4 through a JNK-dependent pathway. Transfer of RBP4-activated APCs into normal mice is sufficient to induce AT inflammation, insulin resistance, and glucose intolerance. Thus, RBP4 causes insulin resistance, at least partly, by activating AT APCs that induce CD4 T cell Th1 polarization and AT inflammation. [Display omitted] •RBP4 causes insulin resistance and innate and adaptive immune system activation•RBP4 activates adipose CD206+ macrophages, which express proinflammatory cytokines•RBP4 activates adipose antigen-presenting cells through a JNK-dependent pathway•Transfer of RBP4-activated antigen-presenting cells induces insulin resistance Elevated RBP4 is associated with increased risk for type 2 diabetes and cardiovascular disease. Moraes-Vieira et al. show that RBP4 directly activates antigen-presenting cells in adipose tissue through a JNK-dependent pathway, leading to adipose tissue inflammation. Transfer of RBP4-activated antigen-presenting cells into normal mice induces insulin resistance.
Publisher: United States: Elsevier Inc
Language: English
Identifier: ISSN: 1550-4131
EISSN: 1932-7420
DOI: 10.1016/j.cmet.2014.01.018
PMID: 24606904
Source: MEDLINE
Open Access: Cell Press Free Archives

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RBP4 Activates Antigen-Presenting Cells, Leading to Adipose Tissue Inflammation and Systemic Insulin Resistance

2014 Elsevier Inc. ;Copyright © 2014 Elsevier Inc. All rights reserved. ;2014 Elsevier Inc. All rights reserved. 2014 ;ISSN: 1550-4131 ;EISSN: 1932-7420 ;DOI: 10.1016/j.cmet.2014.01.018 ;PMID: 24606904

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