IKK-beta links inflammation to obesity-induced insulin resistance.

By M. C. Arkan, A. Hevener, F. Greten, S. Maeda, Zhi-wei Li, J. Long, A. Wynshaw-Boris, G. Poli, Jerrold M. Olefsky, M. Karin. Nature Medicine, 2005

902 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/bc0a387a4ac16c521be62273f27c69f8c3eddd2d

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Citations in the corpus

Weight loss and lipolysis promote a dynamic immune response in murine adipose tissue. (2010, background): “Similarly, myeloid cell–specific deletion of inflammatory pathway–regulating IKK-β reduces obesity-induced inflammation and diet-induced insulin resistance (6, 16).”
Inflammatory Mechanisms in the Regulation of Insulin Resistance (2008, background): “(78) recently presented similar findings in mice lacking either IKKβ in hepatocytes or myeloid cells.”
Regulatory Mechanisms for Adipose Tissue M1 and M2 Macrophages in Diet-Induced Obese Mice (2009, background): “3 besity and insulin resistance are closely associated with a state of low-grade inflammation in adipose tissue, where resident macrophages play important roles (1-9).”
Alternative M2 activation of Kupffer cells by PPARdelta ameliorates obesity-induced insulin resistance. (2008, methodology): “To identify the sites of insulin resistance, WT BMT and PPARd / BMT mice were injected with insulin via their inferior vena cava, and tissues were quickly harvested for biochemical analyses of insulin signaling (Arkan et al., 2005; Cai et al., 2005).”
Obesity induces a phenotypic switch in adipose tissue macrophage polarization. (2007, background): “Moreover, myeloidspecific KO of IκB kinase β (Ikbkb) produced mice with improved insulin sensitivity on HFD (12).”
Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages. (2014, background): “Moreover, targeting pathways that mediate inflammation in the macrophage revealed significant roles for TLR4, JNK, and IKKb in potentiating ATM inflammation and insulin resistance in mice (Arkan et al., 2005; Han et al., 2013; Saberi et al., 2009).”
Inflammation and insulin resistance (2008, background): “As such, these results showed that inactivation of myeloidIkkb activity prevents systemic insulin resistance, most likely by interrupting local paracrine effects between resident macrophages and insulin target tissues [45].”
High-Fat Diet: Bacteria Interactions Promote Intestinal Inflammation Which Precedes and Correlates with Obesity and Insulin Resistance in Mouse (2010, background): “It has been reported that blocking NF-kB in macrophages or liver attenuated inflammatory gene expression and insulin resistance on HF diet [31], c-Jun amino-terminal kinase 1 (JNK1) knockout mice do not become insulin resistant [32] while blocking JNK improves insulin sensitivity [33].”
Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans Published, JLR Papers in Press, September 8, 2005. DOI 10.1194/jlr.M500294-JLR200 (2005, background): “, nuclear factor B) signaling are protected from insulin resistance (10).”
Energy Metabolism in the Liver (2014, unknown): “Liver-speciﬁc deletion of IKK β improves hepatic insulin sensitivity and reduces hepatic gluconeogenesis in HFD-fed mice and ob/ob mice (8).”
TNF-α and adipocyte biology (2007, background): “Despite this, there is ample evidence to support the requirement for the upstream signals that lead to NFκB activation in TNF-α-induced insulin resistance in vitro and in vivo [63,74-76].”
Insulin Resistance: From Mechanisms to Therapeutic Strategies (2021, background): “TNFα also activates inhibitor of nuclear factor κ-B kinase (IKK), and liver- or myeloid cell-specific deletion of IKK protected against hepatic insulin resistance, improved hepatic insulin signaling, and reduced inflammatory cytokine expression [151], which suggested IKK might mediate the role of TN”