Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance.

By Haiyan Xu, Glenn Barnes, Qing Yang, G. Tan, Daseng Yang, C. Chou, Jason Sole, A. Nichols, J. Ross, L. Tartaglia and 1 more. Journal of Clinical Investigation, 2003

6,776 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/8e1989b6b0cff7fe4b1128b79f2f00890b3d8693

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Citations in the corpus

Obesity and Its Metabolic Complications: The Role of Adipokines and the Relationship between Obesity, Inflammation, Insulin Resistance, Dyslipidemia and Nonalcoholic Fatty Liver Disease (2014, background): “many pro-inflammatory chemokines, cytokines and adipokines that are closely related to insulin resistance [5,6,40].”
What We Talk About When We Talk About Fat (2014, positive): “Later work showed that many of these cytokines are produced by macrophages within the fat pad rather than the adipocytes themselves (Weisberg et al., 2003; Xu et al., 2003).”
Inflammation, Defective Insulin Signaling, and Mitochondrial Dysfunction as Common Molecular Denominators Connecting Type 2 Diabetes to Alzheimer Disease (2014, background): “Peripheral (adipose tissue) inflammation is a major trait of diabetes and obesity (107), and both adipocytes and adipose-resident macrophages appear to participate in a cross-talk between the periphery and CNS.”
Adipocytokines: mediators linking adipose tissue, inflammation and immunity (2006, background): “The adipose tissue of obese individuals also contains a large number of macrophages, which are an additional source of soluble mediators in the adipose tissu”
Adipocytokines in Obesity and Metabolic Disease (2014, neutral): “Adiponectin suppresses TNFa production in obese mice (Xu et al. 2003a), and adiponectin-deficient mice have high levels of TNFa in adipose tissue (Maeda et al. 2002).”
Adipose Tissue Macrophage-Derived Exosomal miRNAs Can Modulate In Vivo and In Vitro Insulin Sensitivity. (2017, neutral): “One of the hallmarks of obesity in both humans and rodents is a state of chronic, unresolved inflammation in adipose tissue, liver, and possibly skeletal muscle (Hirosumi et al., 2002; Holland et al., 2011; Hotamisligil et al., 1995, 1996; Shoelson et al., 2003; Xu et al., 2003).”
Insulin resistance: Review of the underlying molecular mechanisms (2018, background): “Obesity‐induced chronic inflammation likely plays an important role in IR in obese subjects (Xu et al., 2003).”
Central leptin regulates total ceramide content and sterol regulatory element binding protein-1C proteolytic maturation in rat white adipose tissue. (2009, background): “Recent studies have shown that a low-grade inflammation in adipose tissue contributes to development of obesity related insulin resistance (12).”
Type 2 diabetes as an inflammatory disease (2011, background): “We now appreciate that adipose tissue macrophages produce a significant proportion of the inflammatory factors that are upregulated by obesit”
Obesity induces a phenotypic switch in adipose tissue macrophage polarization. (2007, background): “ATMs are present in moderate quantities in adipose tissue of lean mice in which inflammatory signals are low or nonexistent (5, 6), and their role there is unclear.”
The cellular and signaling networks linking the immune system and metabolism in disease (2012, background): “Activation of inflammatory pathways has since been observed in all classical insulin target tissues, including fa”
IKK-β links inflammation to obesity-induced insulin resistance (2005, background): “Indeed, it was suggested that chronic inflammation contributes to obesity-induced insulin resistance through macrophage infiltration of fat depot”
Mechanisms of obesity-associated insulin resistance: many choices on the menu. (2007, background): “Furthermore, obesity is characterized by macrophage accumulation in white adipose tissue, which has added another dimension to our understanding of the development of adipose tissue inflammation in obesity (Weisberg et al. 2003; Xu et al. 2003).”