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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Toxicol Appl Pharmacol. 2015 Mar 8;284(3):304–314. doi: 10.1016/j.taap.2015.02.022

Figure 8. Scheme of the working hypothesis.

Figure 8

Previous studies suggest that arsenic toxicity may be a hidden risk factor for developing severe fatty liver disease; indeed this group has shown that arsenic enhances liver injury in a model of NASH (6). Here we propose that the mechanisms underlying enhanced hepatic injury involve changes in both the gut and liver. We propose that HFD and arsenic favor the production of GI tract toxins (e.g. LPS) and increase gut leakiness by altering the GI tract flora. We further propose that HFD and arsenic sensitize the liver to toxic injury caused by gut-derived toxins. Prebiotics have been shown to protect against changes in gut flora and permeability caused by high fat diet (8). Therefore, the aim of this study was to test the hypothesis that the prebiotic oligofructose can protect against hepatic injury caused by HFD and arsenic.