Local and systemic insulin resistance resulting from hepatic activation of IKK-beta and NF-kappaB.

By D. Cai, M. Yuan, Daniel F Frantz, P. A. Meléndez, L. Hansen, Jongsoon Lee, S. Shoelson. Nature Medicine, 2005

1,030 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/50b033a65dd33fc2bcc3bf3bf6e131b87bd9d319

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Citations in the corpus

Obesity in pregnancy stimulates macrophage accumulation and inflammation in the placenta. (2008, background): “This phenotypic heterogeneity strongly suggested that macrophages located in the placenta of obese women may derive from both endogenous and exogenous sources as recently demonstrated in the adipose tissue of mice fed a high fat diet [20].”
Increased Infiltration of Macrophages in Omental Adipose Tissue Is Associated With Marked Hepatic Lesions in Morbid Human Obesity (2006, background): “As macrophage infiltration increases in omental WAT, inflammatory molecules could reach the liver directly through the portal system and act in concert with locally produced proinflammatory factors (33) to increase liver cell apoptosis, a prerequisite for developing fibrosis.”
Non-alcoholic fatty liver disease and its relationship with cardiovascular disease and other extrahepatic diseases (2017, background): “182 183 Receptor activator of NF-κ B, a prototypical activator of NF-κ B, regulates hepatic insulin sensitivity.”
Defining high-fat-diet rat models: metabolic and molecular effects of different fat types. (2006, background): “B activation by arachidonic acid in monocytes and hepatocytes (Camandola et al. 1996, Becuwe et al. 2003), which in turn plays an important role in the pathogenesis of local and systemic insulin resistance (Arkan et al. 2005, Cai et al. 2005).”
Obesity, Inflammation, Toll-Like Receptor 4 and Fatty Acids (2018, background): “However, currently, it is known that there are other tissues involved in meta-inflammation, such as the liver [54], pancreas [55], hypothalamus [56,57], and skeletal muscle [58].”
Visceral Fat Adipokine Secretion Is Associated With Systemic Inflammation in Obese Humans (2007, result): “These findings are consistent with data obtained from LIKK mice, showing that a localized increase in nuclear factor- B and inflammation in the liver can cause peripheral insulin resistance in skeletal muscle (25).”
Biochemistry of adipose tissue: an endocrine organ (2013, background): “Studies show that mRNA expression levels of TNF-α in adipose tissue in obesity is strongly implicated in the pathogenesis of insulin resistance; this is because it has been demonstrated that TNF-α can impair insulin signaling in hepatocytes and adipose tissue [29].”
Increased Hepatic and Circulating Interleukin-6 Levels in Human Nonalcoholic Steatohepatitis (2008, background): “Furthermore, plasma IL-6 levels increased in parallel to hepatic IL-6 expression in these mice, and systemic neutralization of IL-6 restored insulin sensitivity to near-normal levels (13).”
Inflammation, stress, and diabetes. (2005, unknown): “Activation of IKK in liver and myeloid cells appears to contribute to obesity-induced insulin resistance, though this pathway may not be as important in muscle (62–64).”
Inflammatory Mechanisms in the Regulation of Insulin Resistance (2008, background): “(77) created a stage of chronic, subacute inflammation in the liver in a transgenic mouse model by selective hepatocellular activation of NF-κB causing continuous lowlevel expression of IKKβ.”
Recent advances in the relationship between obesity, inflammation, and insulin resistance. (2006, background): “Accordingly, selective inhibition of the NF-jB function in liver and adipose tissue protects against insulin resistance in nutritional and genetic animal models of obesity [86].”
High‐fat Diets: Modeling the Metabolic Disorders of Human Obesity in Rodents (2007, background): “Very recent work has drawn attention to the activation of nuclear factor B by HF diets in the liver, which might contribute both to the development of non-alcoholic inflammatory hepatic disease and diet-induced disorders of hepatic glucose metabolism (91).”
Impact of the gut microbiota on inflammation, obesity, and metabolic disease (2016, background): “have shown that activation of effector molecules of inflammation contributes to desensitizing insulin signaling pathways [24].”