Obesity induces a phenotypic switch in adipose tissue macrophage polarization.

By C. Lumeng, Jennifer L Bodzin, Alan R. Saltiel. Journal of Clinical Investigation, 2007

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View Paper: https://www.semanticscholar.org/paper/90f8ef41fcb2fac6042be52196b953041c36a568

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Citations in the corpus

Macrophage plasticity and polarization: in vivo veritas. (2012, positive): “In contrast, M1-like ATMs drive obesity-associated inflammation and insulin resistance (107).”
The cellular and signaling networks linking the immune system and metabolism in disease (2012, background): “In obesity, CD11c + ATMs are considered to be M1-like or CAM cell types, whereas the resident macrophages are noninflammatory and CD11c − and are classified as M2-like or as AAM cell type”
The Phagocytic Function of Macrophage-Enforcing Innate Immunity and Tissue Homeostasis (2017, background): “Almost all infiltrating macrophages are M1 macrophages, and the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α and IL-6 is aggravated [83].”
Adipocyte-derived Th2 cytokines and myeloid PPARdelta regulate macrophage polarization and insulin sensitivity. (2008, background): “…as TNFa has been shown to interfere with glucose metabolism by downregulation of GLUT4, to inhibit insulin sensitivity through JNK activation (Hirosumi et al., 2002; Lumeng et al., 2007b; Ruan et al., 2002), and to cause lipolysis by suppression of perilipin expression (Laurencikiene et al., 2007).”
The NALP3/NLRP3 Inflammasome Instigates Obesity-Induced Autoinflammation and Insulin Resistance (2011, background): “The activation of classically activated M1 macrophages at the expense of anti-inflammatory M2 macrophages has been causally linked to the development of adipose tissue inflammation and metabolic syndrom”
The Metabolic Signature of Macrophage Responses (2019, background): “Finally, M2d macrophages, also known as tumor-associated macrophages (TAMs), are induced by TLR ligands and A2 adenosine receptor (A2R) agonists, or by IL-6; they secrete high levels of IL-10, TGF-β, and VEGF and low IL12, TNF-α, and IL-1β, and contribute to tumor angiogenesis, growth and metastasis”
Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages. (2014, background): “It has been proposed that during weight gain macrophages undergo a ''phenotypic switch'' from an anti-inflammatory M2 phenotype to a proinflammatory M1 state, a conversion that has been linked to the emergence of systemic insulin resistance (Lumeng et al., 2007).”
Macrophage-mediated inflammation in metabolic disease (2011, background): “Adipose tissue macrophages in lean animals have an alternatively activated (M2) phenotype (ARG1 + CD206 + CD301 + ), are less inflammatory than classically activated macrophages and are uniformly dispersed throughout the adipose tissue, whereas adipose tissue macrophages of obese mice have a pro-i”
B Lymphocytes Promote Insulin Resistance through Modulation of T Lymphocytes and Production of Pathogenic IgG Antibody (2011, background): “Classically activated, or CD11c + CD206 − M1 macrophages, are elevated in VAT of DIO mice and produce proinflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 (refs”
Inflammation and insulin resistance (2008, background): “have shown that Il-10 treated 3T3L1 adipocytes are protected from Tnf-induced cellular insulin resistance [41].”
Adipocyte Death, Adipose Tissue Remodeling, and Obesity Complications (2007, background): “However, the relationship between this obesityassociated ATM “phenotypic switch” (12) and the development and progression of obesity complications is unclear (16,17).”