Adipose tissue macrophages

• Published in: Immunology Letters 2007-10, Vol.112 (2), p.61-67
• Main Authors: Zeyda, Maximilian, Stulnig, Thomas M
• Format: Article
• Language: English
• Subjects: Adipose Tissue - metabolism; Adipose Tissue - pathology; Allergy and Immunology; Alternatively activated macrophages; Animals; Chronic Disease; Cytokines - metabolism; Diabetes Mellitus, Type 2 - etiology; Diabetes Mellitus, Type 2 - metabolism; Humans; Inflammation; Inflammation Mediators - metabolism; Insulin Resistance; Macrophage Activation; Macrophages - metabolism; Macrophages - pathology; Metabolic Syndrome - etiology; Metabolic Syndrome - metabolism; Mice; Mice, Obese; Obesity; Obesity - complications; Obesity - metabolism; Obesity - pathology; Panniculitis - complications; PPAR gamma - deficiency; PPAR gamma - metabolism
• ISSN: 0165-2478; 1879-0542; 1365-2567
• DOI: 10.1016/j.imlet.2007.07.003

Abstract It is now broadly accepted that low-grade chronic inflammation associated with obesity leads to the onset of insulin resistance and type 2 diabetes mellitus. Obesity-associated inflammation is characterized by an increased abundance of macrophages in adipose tissue along with production of inflammatory cytokines. Adipose tissue macrophages (ATMs) are suspected to be the major source of inflammatory mediators such as TNF-α and IL-6 that interfere with adipocyte function by inhibiting insulin action. However, ATMs phenotypically resemble alternatively activated (M2) macrophages and are capable of anti-inflammatory mediator production challenging the concept that ATMs are simply the “bad guys” in obese adipose tissue. Triggers promoting ATM recruitment, ATM functions and dysfunctions, and stimuli and molecular mechanisms that drive them into becoming detrimental to their environment are subject to current research. Strategies to interfere with ATM recruitment and adverse activation could give rise to novel options for treatment and prevention of insulin resistance and type 2 diabetes mellitus.