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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: Curr Opin Support Palliat Care. 2014 Dec;8(4):321–327. doi: 10.1097/SPC.0000000000000091

Figure 2. Representative figure demonstrating the systemic effect of IL - 6 dependent cachexia in vivo.

Figure 2

IL - 6 source mainly from the tumor and immune cells like macrophages affects various organs like adipose, muscle liver and gut with contrasting effects. Adipose tissue undergoes rapid lipolysis under chronic IL-6 conditions [6, 13, 19]. Muscle demonstrates activation of inflammatory and degradation pathways with a suppression of protein synthesis signaling. The liver demonstrates hypertrophy, an upregulation of innate inflammatory pathways, with a possible suppression of adaptive responses and disruption in lipid signaling. The gut is affected by chronic IL - 6 exposure with increased gut permeability possible due to a disruption in tight junction proteins and anemia. Both increased gut permeability and liver dysfunction may contribute to endotoxemia seen in the later stages of cachexia. Abbreviations: TJ = Tight junctions, APR = Acute Phase Response, VLDL = Very low density lipoproteins. Images in the figure were downloaded and adapted from an online image library: dreamstime royaltyfree stock photos. http://www.dreamstime.com/photos-images.html.