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Nonalcoholic fatty liver disease and alcohol-related liver disease: From clinical aspects to pathophysiological insights
Two major causes of steatohepatitis are alcohol and metabolic syndrome. Although the underlying causes of alcohol-related liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH) differ, there are certain similarities in terms of the mode of disease progre...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Korean Association for the Study of the Liver
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7641569/ https://www.ncbi.nlm.nih.gov/pubmed/33053942 http://dx.doi.org/10.3350/cmh.2020.0202 |
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author | Ikejima, Kenichi Kon, Kazuyoshi Yamashina, Shunhei |
author_facet | Ikejima, Kenichi Kon, Kazuyoshi Yamashina, Shunhei |
author_sort | Ikejima, Kenichi |
collection | PubMed |
description | Two major causes of steatohepatitis are alcohol and metabolic syndrome. Although the underlying causes of alcohol-related liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH) differ, there are certain similarities in terms of the mode of disease progression and underlying pathophysiological mechanisms. Further, excessive alcohol consumption is often seen in patients with metabolic syndrome, and alcoholic hepatitis exacerbation by comorbidity with metabolic syndrome is an emerging clinical problem. There are certain ethnic differences in the development of both NAFLD and ALD. Especially, Asian populations tend to be more susceptible to NAFLD, and genetic polymorphisms in patatin-like phospholipase domain-containing 3 (PNPLA3) play a key role in both NAFLD and ALD. From the viewpoint of pathophysiology, cellular stress responses, including autophagy and endoplasmic reticulum (ER) stress, are involved in the development of cellular injury in steatohepatitis. Further, gut-derived bacterial products and innate immune responses in the liver most likely play a profound role in the pathogenesis of both ALD and NASH. Though the recent progress in the treatment of viral hepatitis has reduced the prevalence of viral-related development of hepatocellular carcinoma (HCC), non-viral HCC is increasing. Alcohol and metabolic syndrome synergistically exacerbate progression of steatohepatitis, resulting in carcinogenesis. The gut-liver axis is a potential therapeutic and prophylactic target for steatohepatitis and subsequent carcinogenesis. |
format | Online Article Text |
id | pubmed-7641569 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | The Korean Association for the Study of the Liver |
record_format | MEDLINE/PubMed |
spelling | pubmed-76415692020-11-13 Nonalcoholic fatty liver disease and alcohol-related liver disease: From clinical aspects to pathophysiological insights Ikejima, Kenichi Kon, Kazuyoshi Yamashina, Shunhei Clin Mol Hepatol Review Two major causes of steatohepatitis are alcohol and metabolic syndrome. Although the underlying causes of alcohol-related liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH) differ, there are certain similarities in terms of the mode of disease progression and underlying pathophysiological mechanisms. Further, excessive alcohol consumption is often seen in patients with metabolic syndrome, and alcoholic hepatitis exacerbation by comorbidity with metabolic syndrome is an emerging clinical problem. There are certain ethnic differences in the development of both NAFLD and ALD. Especially, Asian populations tend to be more susceptible to NAFLD, and genetic polymorphisms in patatin-like phospholipase domain-containing 3 (PNPLA3) play a key role in both NAFLD and ALD. From the viewpoint of pathophysiology, cellular stress responses, including autophagy and endoplasmic reticulum (ER) stress, are involved in the development of cellular injury in steatohepatitis. Further, gut-derived bacterial products and innate immune responses in the liver most likely play a profound role in the pathogenesis of both ALD and NASH. Though the recent progress in the treatment of viral hepatitis has reduced the prevalence of viral-related development of hepatocellular carcinoma (HCC), non-viral HCC is increasing. Alcohol and metabolic syndrome synergistically exacerbate progression of steatohepatitis, resulting in carcinogenesis. The gut-liver axis is a potential therapeutic and prophylactic target for steatohepatitis and subsequent carcinogenesis. The Korean Association for the Study of the Liver 2020-10 2020-10-01 /pmc/articles/PMC7641569/ /pubmed/33053942 http://dx.doi.org/10.3350/cmh.2020.0202 Text en Copyright © 2020 by The Korean Association for the Study of the Liver This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Ikejima, Kenichi Kon, Kazuyoshi Yamashina, Shunhei Nonalcoholic fatty liver disease and alcohol-related liver disease: From clinical aspects to pathophysiological insights |
title | Nonalcoholic fatty liver disease and alcohol-related liver disease: From clinical aspects to pathophysiological insights |
title_full | Nonalcoholic fatty liver disease and alcohol-related liver disease: From clinical aspects to pathophysiological insights |
title_fullStr | Nonalcoholic fatty liver disease and alcohol-related liver disease: From clinical aspects to pathophysiological insights |
title_full_unstemmed | Nonalcoholic fatty liver disease and alcohol-related liver disease: From clinical aspects to pathophysiological insights |
title_short | Nonalcoholic fatty liver disease and alcohol-related liver disease: From clinical aspects to pathophysiological insights |
title_sort | nonalcoholic fatty liver disease and alcohol-related liver disease: from clinical aspects to pathophysiological insights |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7641569/ https://www.ncbi.nlm.nih.gov/pubmed/33053942 http://dx.doi.org/10.3350/cmh.2020.0202 |
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