Inflammatory pathways and insulin action

By G. Hotamisligil. International Journal of Obesity, 2003

741 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Physiology

View Paper: https://www.semanticscholar.org/paper/83e889e82aff11a293f7a440313780cd2b6e41aa

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Citations in the corpus

Hypoxia and adipose tissue function and dysfunction in obesity. (2013, background): “There has also been considerable interest in the adipokines involved in the inflammatory response, this reflecting the link between inflammation in adipose tissue and the development of obesity-associated diseases (80, 81, 158, 167, 198).”
Local and systemic insulin resistance resulting from hepatic activation of IKK-β and NF-κB (2005, methodology): “We isolated IKK complexes from mouse liver lysates using anti-IKK-γ antibodies (PharMingen) coupled to protein A-Sepharose, and conducted in vitro kinase assays at 30 °C by adding [γ-32P]ATP and 2 μg of GST-IκBα (1-54)12.”
Interleukin-6 Increases Insulin-Stimulated Glucose Disposal in Humans and Glucose Uptake and Fatty Acid Oxidation In Vitro via AMP-Activated Protein Kinase (2006, background): “Diabetes 55:2688–2697, 2006 The pathogenesis of type 2 diabetes is not fully understood, but growing evidence links this disease to a state of chronic inflammation (1), which occurs in tissue such as liver, adipose, and skeletal muscle and results in the secretion of inflammatory cytokines such as r”
Psoriasis and systemic inflammatory diseases: potential mechanistic links between skin disease and co-morbid conditions. (2010, background): “Signal transduction pathways linking inflammation and insulin resistance through inhibition of phosphorylation of insulin signaling include NF-kB, c-Jun N-terminal kinase, and endothelial reticulum stress, such as obesity (Hotamisligil, 2003; Ozcan et al., 2004; Arkan et al., 2005; Cai et al., 2005)”
Inhibition of ceramide synthesis ameliorates glucocorticoid-, saturated-fat-, and obesity-induced insulin resistance. (2007, background): “First, increased adipose tissue mass may trigger the synthesis and/or secretion of glucocorticoids (Hermanowski-Vosatka et al., 2005) or inflammatory cytokines (e.g., tumor necrosis factor a [TNFa]) (Hotamisligil, 2003) that inhibit insulin action in peripheral tissues.”
Mechanisms of obesity-associated insulin resistance: many choices on the menu. (2007, background): “Adipose tissue expression of TNF is increased in obese rodents and humans and positively correlated with adiposity and insulin resistance (Hotamisligil et al. 1993; Fernandez-Real and Ricart 2003; Hotamisligil 2003; Ruan and Lodish 2003).”
Consumption of a fat-rich diet activates a proinflammatory response and induces insulin resistance in the hypothalamus. (2005, methodology): “In recent years, a bulk of evidence has been obtained to show that certain proinflammatory cytokines, produced by the adipose tissue, participate in the induction of insulin resistance in tissues that act as traditional targets for insulin action (14, 15).”