1. NF-κB, Inflammation, and Metabolic Disease
Rebecca G. Baker, Matthew S. Hayden, Sankar Ghosh 
Cell Metabolism 
Volume 13, Issue 1, Pages (January 2011)
DOI: /j.cmet
Copyright © 2011 Elsevier Inc. Terms and Conditions

2. Figure 1
Inflammatory Triggers Activate Expression of Proinflammatory Genes through IKK and NF-κB
After engagement of Toll-like receptors and cytokine receptors, signaling through MyD88 and death domain adaptor molecules (respectively) and then via TRAFs results in phosphorylation of IKK and activation of the IKK complex kinase activity. NF-κB is constitutively bound to IκB molecules which confine its localization to the cytosol. IKK complex phosphorylation of serine residues on IκB promotes its polyubiquitination and degradation, thereby freeing NF-κB to enter the nucleus and activate transcription of target genes.
Cell Metabolism  , 11-22DOI: ( /j.cmet )
Copyright © 2011 Elsevier Inc. Terms and Conditions

3. Figure 2
Overweight and Obesity Induces Activation of Inflammatory Mediators in Adipocytes and Infiltrating Macrophage Cells
Metabolism of excess nutrients imposes stress on adipose tissue. Production of proinflammatory cytokines by adipocytes and adipocyte hypertrophy and expiration recruits M1 proinflammatory macrophages into the adipose tissue. Proinflammatory signaling in central nervous system and macrophage-derived cytokines promote systemic dysregulation of leptin signaling and perturbed energy balance.
Cell Metabolism  , 11-22DOI: ( /j.cmet )
Copyright © 2011 Elsevier Inc. Terms and Conditions

4. Figure 3 TLR and ER Stress Responses in Insulin Resistance
Signaling from cytokine receptors and Toll-like receptors on the cell surface, as well as ER stress, can activate the IKK complex and NF-κB to activate expression of proinflammatory cytokines and disable insulin signaling. Defective insulin signaling contributes to insulin resistance and the development of type 2 diabetes.
Cell Metabolism  , 11-22DOI: ( /j.cmet )
Copyright © 2011 Elsevier Inc. Terms and Conditions

5. Figure 4 Macrophage Cells Are Central Mediators of Insulin Resistance
Nutrient excess is sensed in peripheral metabolic tissues to result in production of proinflammatory cytokines IL-6, IL-1, and TNF-α. These cytokines drive macrophage activation and propagation of proinflammatory signals throughout the organism.
Cell Metabolism  , 11-22DOI: ( /j.cmet )
Copyright © 2011 Elsevier Inc. Terms and Conditions

6. Figure 5
NF-κB Mediates Proinflammatory Signaling in Endothelia and Leukocytes that Drives Atherogenesis
Proinflammatory signaling networks through NF-κB in vascular endothelia respond to deposition of oxidized lipoproteins by expression of adhesion molecules on the cell surface and leukocyte cytokines. Circulating monocytes are arrested at the site of inflammation and differentiate into cytokine-producing macrophage cells. Macrophage cells also consume lipids on the vascular wall swelling into foam cells that nucleate the atherosclerotic plaque. Continued recruitment, activation of leukocytes, lipid consumption, and cell death results in the formation of a large atherosclerotic lesion impairing arterial blood flow and promoting thrombosis.
Cell Metabolism  , 11-22DOI: ( /j.cmet )
Copyright © 2011 Elsevier Inc. Terms and Conditions