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. 2017 Dec 13;5(3):367–398. doi: 10.1016/j.jcmgh.2017.11.016

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© 2018 The Authors

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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Nrf2-dependent mechanisms by which TBE-31 suppresses insulin resistance, NASH and cirrhosis. (A) The various mechanisms by which consumption of a high-fat and high-fructose diet is believed to drive hepatic steatosis, NASH, and cirrhosis.4, 5, 8 (B) The processes by which we envisage pharmacologic activation of Nrf2 inhibits and/or reverses liver disease caused by consumption of a diet enriched with high-fat and high-fructose foodstuffs. For further information see Results and Discussion sections. HSC, hepatic stellate cell.

Nrf2-dependent mechanisms by which TBE-31 suppresses insulin resistance, NASH and cirrhosis. (A) The various mechanisms by which consumption of a high-fat and high-fructose diet is believed to drive hepatic steatosis, NASH, and cirrhosis.4, 5, 8 (B) The processes by which we envisage pharmacologic activation of Nrf2 inhibits and/or reverses liver disease caused by consumption of a diet enriched with high-fat and high-fructose foodstuffs. For further information see Results and Discussion sections. HSC, hepatic stellate cell.