Prevention of fat-induced insulin resistance by salicylate.

By Jason K. Kim, Yoon-Jung Kim, Jonathan J. Fillmore, Yan Chen, Irene K. Moore, Jongsoon Lee, M. Yuan, Zhi-wei Li, Michael Karin, P. Perret and 2 more. Journal of Clinical Investigation, 2001

745 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/085bacfc899d8b154b38fa7a714d3fb7f2eab789

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Citations in the corpus

Increased Inflammatory Properties of Adipose Tissue Macrophages Recruited During Diet-Induced Obesity (2007, background): “Anti-inflammatory therapies and the disruption of genes important in proinflammatory responses, such as I B kinase- (IKK ), improve insulin sensitivity in obese animals (2,3).”
Cellular and Molecular Players in Adipose Tissue Inflammation in the Development of Obesity-induced Insulin Resistance (2013, positive): “These clinical but still observational studies were then supported by preclinical studies showing that obesity activates inflammation via the IKKβ/NFκB pathway and that inhibition of this pathway by genetic deletion of IKKβ or pharmacological inhibitors of this pathway (a high dose of salicylates or”
Dietary factors and low-grade inflammation in relation to overweight and obesity (2011, positive): “The longest experience is with the use of salicylates which are weak inhibitors of IkB kinase b and of serine phosphorylation of IRS proteins((143,144)).”
Are oxidative stress-activated signaling pathways mediators of insulin resistance and beta-cell dysfunction? (2003, background): “In addition, salicylates inhibit IKK- activity and restore insulin sensitivity, both in vitro and in vivo (56,59).”
Interleukin-6 induces cellular insulin resistance in hepatocytes. (2002, background): “Shoelson and coworkers (47,48) have provided evidence that salicylates can alleviate obesity-dependent and TNF–induced insulin resistance.”
Inflammation and insulin resistance (2008, background): “They also performed lipid infusions in Ikkb heterozygous knockout mice (Ikkb ) and reported similar improvements in insulin sensitivity when compared to wildtype controls [30].”
A ceramide-centric view of insulin resistance. (2012, background): “TLRs signal through IkKb and NFkB, and the Shoelson group has identified this pathway as an important contributor to impaired glucose tolerance (Cai et al., 2005; Donath and Shoelson, 2011; Kim et al., 2001; Yuan et al., 2001).”