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. 2020 Mar 2;9(3):590. doi: 10.3390/cells9030590

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Interaction of liver damage with extra-hepatic organs. NAFLD is influences by interaction with other organs/tissues. Adipose tissue disarrangement (expansion/inflammation) induces increased Free Fatty Acid (FFA) afflux to the liver and insulin resistance; moreover, it releases several pro-inflammatory cytokines and modifies the adipocytokine balance. Dysbiosis in the gut results in translocation of endotoxins (i.e., lipopolysaccharides) to the liver and the subsequent activation of the Toll-like Receptor (TLR) pathway in the liver. In turn, liver with NAFLD/NASH can influence atherosclerosis (plaque formation) by several mechanisms, including, but not limited to, systemic inflammation and oxidative stress increase.