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Fig. 7 | Nutrition & Metabolism

Fig. 7

From: Regulatory landscape of AGE-RAGE-oxidative stress axis and its modulation by PPARγ activation in high fructose diet-induced metabolic syndrome

Fig. 7

Diagram depicting the AROS axis and summarizing our results. The metabolic syndrome is probably generated through the activation of the AROS axis [8]. Reactive sugar aldehydes form adducts with proteins (AGEs) which then bind to their specific receptor (RAGE, localized in a specialized membrane compartment, the lipid raft), initiating the RAGE signalling cascade. As a result, enzymes generating reactive oxygen species (ROS) are activated, which in turn activates NF-kB translocation from cytosol to nucleus, ultimately altering expression of numerous genes, including upregulation of pro-inflammatory cytokines (TNF-α, IL-6). The resulting inflamation, in turn, is responsible for additional tissue oxidative stress (AOPP production) [49], lipoxidation and HNE production [913], all contributing to a further elevation and perpetuation of both molecular/cellular damage and the inflammatory response [50]. Activation of PPARγ binding by RGZ also leads to altered expression of numerous genes, including upregulation of a soluble isoform of RAGE able to bind extracellular AGEs for clearance from the plasma [51], thereby attenuating (at least in part) the AROS axis. Summary of results from this study: (i) upward red arrows = increased levels of the indicated measured parameters in response to HFD; (ii) downward green arrows = decreased levels of the indicated measured parameters in response to RGZ

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