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Thyroid hormone-mediated autophagy and mitochondrial turnover in NAFLD

Non-alcoholic fatty liver disease (NAFLD) is a fast-growing silent epidemic that is present in both developed and developing countries. Initially thought as a benign deposition of lipids in the liver, it now has been shown to be a major risk factor for type II diabetes and one of the leading causes...

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Autores principales: Sinha, Rohit Anthony, Yen, Paul M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4950712/
https://www.ncbi.nlm.nih.gov/pubmed/27437098
http://dx.doi.org/10.1186/s13578-016-0113-7
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author Sinha, Rohit Anthony
Yen, Paul M.
author_facet Sinha, Rohit Anthony
Yen, Paul M.
author_sort Sinha, Rohit Anthony
collection PubMed
description Non-alcoholic fatty liver disease (NAFLD) is a fast-growing silent epidemic that is present in both developed and developing countries. Initially thought as a benign deposition of lipids in the liver, it now has been shown to be a major risk factor for type II diabetes and one of the leading causes of cirrhosis. Recent findings suggest that dysregulation of mitochondrial homeostasis and autophagy play critical roles in the hepatocyte injury and insulin resistance of NAFLD. Thyroid hormone (TH) is a major stimulator of hepatic autophagy and mitochondrial function. Decreased TH action has been associated with NAFLD in man. In this review, we highlight some of the new discoveries that demonstrate the roles of TH in hepatic mitochondrial homeostasis via mitophagy and their implications for NAFLD.
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spelling pubmed-49507122016-07-20 Thyroid hormone-mediated autophagy and mitochondrial turnover in NAFLD Sinha, Rohit Anthony Yen, Paul M. Cell Biosci Review Non-alcoholic fatty liver disease (NAFLD) is a fast-growing silent epidemic that is present in both developed and developing countries. Initially thought as a benign deposition of lipids in the liver, it now has been shown to be a major risk factor for type II diabetes and one of the leading causes of cirrhosis. Recent findings suggest that dysregulation of mitochondrial homeostasis and autophagy play critical roles in the hepatocyte injury and insulin resistance of NAFLD. Thyroid hormone (TH) is a major stimulator of hepatic autophagy and mitochondrial function. Decreased TH action has been associated with NAFLD in man. In this review, we highlight some of the new discoveries that demonstrate the roles of TH in hepatic mitochondrial homeostasis via mitophagy and their implications for NAFLD. BioMed Central 2016-07-19 /pmc/articles/PMC4950712/ /pubmed/27437098 http://dx.doi.org/10.1186/s13578-016-0113-7 Text en © The Author(s) 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Sinha, Rohit Anthony
Yen, Paul M.
Thyroid hormone-mediated autophagy and mitochondrial turnover in NAFLD
title Thyroid hormone-mediated autophagy and mitochondrial turnover in NAFLD
title_full Thyroid hormone-mediated autophagy and mitochondrial turnover in NAFLD
title_fullStr Thyroid hormone-mediated autophagy and mitochondrial turnover in NAFLD
title_full_unstemmed Thyroid hormone-mediated autophagy and mitochondrial turnover in NAFLD
title_short Thyroid hormone-mediated autophagy and mitochondrial turnover in NAFLD
title_sort thyroid hormone-mediated autophagy and mitochondrial turnover in nafld
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4950712/
https://www.ncbi.nlm.nih.gov/pubmed/27437098
http://dx.doi.org/10.1186/s13578-016-0113-7
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