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Role of the AMPK/SIRT1 pathway in non-alcoholic fatty liver disease (Review)

Non-alcoholic fatty liver disease (NAFLD) is an increasingly prevalent ailment worldwide. Moreover, de novo lipogenesis (DNL) is considered a critical factor in the development of NAFLD; hence, its inhibition is a promising target for the prevention of fatty liver disease. There is evidence to indic...

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Autores principales: Anggreini, Putri, Kuncoro, Hadi, Sumiwi, Sri Adi, Levita, Jutti
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9827347/
https://www.ncbi.nlm.nih.gov/pubmed/36562343
http://dx.doi.org/10.3892/mmr.2022.12922
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author Anggreini, Putri
Kuncoro, Hadi
Sumiwi, Sri Adi
Levita, Jutti
author_facet Anggreini, Putri
Kuncoro, Hadi
Sumiwi, Sri Adi
Levita, Jutti
author_sort Anggreini, Putri
collection PubMed
description Non-alcoholic fatty liver disease (NAFLD) is an increasingly prevalent ailment worldwide. Moreover, de novo lipogenesis (DNL) is considered a critical factor in the development of NAFLD; hence, its inhibition is a promising target for the prevention of fatty liver disease. There is evidence to indicate that AMP-activated protein kinase (AMPK) and sirtuin 1 (SIRT1) may play a crucial role in DNL and are the regulatory proteins in type 2 diabetes mellitus, obesity and cardiovascular disease. Therefore, AMPK and SIRT1 may be promising targets for the treatment of NAFLD. The present review article thus aimed to summarize the findings of clinical studies published during the past decade that suggested the beneficial effects of AMPK and SIRT1, using their specific activators and their combined effects on fatty liver disease.
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spelling pubmed-98273472023-01-13 Role of the AMPK/SIRT1 pathway in non-alcoholic fatty liver disease (Review) Anggreini, Putri Kuncoro, Hadi Sumiwi, Sri Adi Levita, Jutti Mol Med Rep Review Non-alcoholic fatty liver disease (NAFLD) is an increasingly prevalent ailment worldwide. Moreover, de novo lipogenesis (DNL) is considered a critical factor in the development of NAFLD; hence, its inhibition is a promising target for the prevention of fatty liver disease. There is evidence to indicate that AMP-activated protein kinase (AMPK) and sirtuin 1 (SIRT1) may play a crucial role in DNL and are the regulatory proteins in type 2 diabetes mellitus, obesity and cardiovascular disease. Therefore, AMPK and SIRT1 may be promising targets for the treatment of NAFLD. The present review article thus aimed to summarize the findings of clinical studies published during the past decade that suggested the beneficial effects of AMPK and SIRT1, using their specific activators and their combined effects on fatty liver disease. D.A. Spandidos 2022-12-21 /pmc/articles/PMC9827347/ /pubmed/36562343 http://dx.doi.org/10.3892/mmr.2022.12922 Text en Copyright: © Anggreini et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Review
Anggreini, Putri
Kuncoro, Hadi
Sumiwi, Sri Adi
Levita, Jutti
Role of the AMPK/SIRT1 pathway in non-alcoholic fatty liver disease (Review)
title Role of the AMPK/SIRT1 pathway in non-alcoholic fatty liver disease (Review)
title_full Role of the AMPK/SIRT1 pathway in non-alcoholic fatty liver disease (Review)
title_fullStr Role of the AMPK/SIRT1 pathway in non-alcoholic fatty liver disease (Review)
title_full_unstemmed Role of the AMPK/SIRT1 pathway in non-alcoholic fatty liver disease (Review)
title_short Role of the AMPK/SIRT1 pathway in non-alcoholic fatty liver disease (Review)
title_sort role of the ampk/sirt1 pathway in non-alcoholic fatty liver disease (review)
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9827347/
https://www.ncbi.nlm.nih.gov/pubmed/36562343
http://dx.doi.org/10.3892/mmr.2022.12922
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