MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity.

By Hajime Kanda, Sanshiro Tateya, Y. Tamori, K. Kotani, K. Hiasa, R. Kitazawa, S. Kitazawa, Hitoshi Miyachi, S. Maeda, K. Egashira and 1 more. Journal of Clinical Investigation, 2006

2,622 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Physiology

View Paper: https://www.semanticscholar.org/paper/633420da240097946bd231288e992d2ed8460399

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Citations in the corpus

Tissue-Resident Macrophage Ontogeny and Homeostasis. (2016, background): “and to CCR2-mediated recruitment of monocytes and differentiation into macrophages (Kanda et al., 2006; Weisberg et al., 2006), little is known about the ontogeny of these cells in healthy”
Macrophage plasticity and polarization: in vivo veritas. (2012, neutral): “(101, 103, 104) and by the macrophage-derived apoptosis inhibitor of macrophages (AIM) (105).”
Adipokines in inflammation and metabolic disease (2011, background): “The expression of CCL2 (also known as MCP1) has been shown to be increased in adipose tissues under conditions of glucose deprivatio”
Adipocytokines: mediators linking adipose tissue, inflammation and immunity (2006, background): “CCL2, produced by adipocytes, has recently been identified as a potential factor contributing to macrophage infiltration into adipose tissu”
Insulin receptor signaling in normal and insulin-resistant states. (2014, background): “Deletion of MCP-1 or its receptor CCR2 improves insulin sensitivity and ameliorates inflammation in mice (Kanda et al. 2006; Weisberg et al. 2006).”
Obesity induces a phenotypic switch in adipose tissue macrophage polarization. (2007, background): “Mice with targeted deletions in the genes for monocyte chemoattractant protein–1 (Mcp1/Ccl2) and its receptor C-C motif chemokine receptor 2 (Ccr2) both have decreased ATM content, decreased inflammation in fat, and protection from high-fat diet–induced (HFD-induced) insulin resistance (9, 10).”
Adipose Tissue Remodeling: Its Role in Energy Metabolism and Metabolic Disorders (2016, background): “org April 2016 | Volume 7 | Article 30 receptor CCR2-deficient mice are protected against macrophage accumulation and inflammatory responses in adipose tissues and are resistant to DIO-induced insulin resistance (138, 139).”
Adipose tissue plasticity in health and disease (2022, background): “Similarly, reducing macrophage recruitment into adipose tissue ameliorates metabolic complications in high-fat-fed mice (Kanda et al., 2006; Weisberg et al., 2006).”
Increased oxidative stress in obesity: implications for metabolic syndrome, diabetes, hypertension, dyslipidemia, atherosclerosis, and cancer. (2013, background): “[44] Kanda H, Tateya S, Tamori Y, Kotani K, Hiasa K, Kitazawa R, et al.”
Normalization of Obesity-Associated Insulin Resistance through Immunotherapy: CD4+ T Cells Control Glucose Homeostasis (2009, background): “The roles of fat-resident macrophages in obesity-induced insulin-resistance differ, with VAT being the principal driver of metabolic syndrome progressio”
Obesity, inflammation, and atherosclerosis (2009, background): “MCP-1-deficient and CCR2-deficient animals present reduced numbers of adipose tissue macrophages, less fat inflammation, and greater insulin sensitivity, which supports the importance of MCP-1 and CCR2 in macrophage migration to obese adipose tissue, and the relevance of macrophages in the metabolic”