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Analysis of N6-Methyladenosine Methylation Modification in Fructose-Induced Non-Alcoholic Fatty Liver Disease

Improvements in living standards have led to non-alcoholic fatty liver disease (NAFLD), one of the most common chronic liver diseases worldwide. Recent studies have shown that N6-methyladenosine (m6A), a type of RNA modification, is strongly associated with many important biological processes. Howev...

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Autores principales: Luo, Yunchen, Zhang, Zhijian, Xiang, Liping, Zhou, Bing, Wang, Xuejiao, Lin, Yi, Ding, Xiaoying, Liu, Fang, Lu, Yan, Peng, Yongde
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8688819/
https://www.ncbi.nlm.nih.gov/pubmed/34950107
http://dx.doi.org/10.3389/fendo.2021.780617
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author Luo, Yunchen
Zhang, Zhijian
Xiang, Liping
Zhou, Bing
Wang, Xuejiao
Lin, Yi
Ding, Xiaoying
Liu, Fang
Lu, Yan
Peng, Yongde
author_facet Luo, Yunchen
Zhang, Zhijian
Xiang, Liping
Zhou, Bing
Wang, Xuejiao
Lin, Yi
Ding, Xiaoying
Liu, Fang
Lu, Yan
Peng, Yongde
author_sort Luo, Yunchen
collection PubMed
description Improvements in living standards have led to non-alcoholic fatty liver disease (NAFLD), one of the most common chronic liver diseases worldwide. Recent studies have shown that N6-methyladenosine (m6A), a type of RNA modification, is strongly associated with many important biological processes. However, the relationship between m6A methylation modifications and NAFLD remains poorly understood. In the present study, through methylated RNA immunoprecipitation sequencing and RNA transcriptome sequencing in high fructose diet-induced NAFLD mice, we found that hypermethylation-encoding genes were mainly enriched in lipid metabolism processes. We identified 266 overlapping and differentially expressed genes (DEGs) that changed at both the mRNA expression level and m6A modification level. Among them, 193 genes displayed increased expression and m6A modification, indicating that m6A RNA modifications tend to be positively correlated with NAFLD. We further compared the high fructose diet-induced NAFLD mouse model with leptin receptor-deficient mice and found that DEGs enriched in the lipid metabolism pathway were up-regulated in both groups. In contrast, DEGs associated with the immune inflammatory response were up-regulated in the high fructose diet group, but down-regulated in leptin receptor-deficient mice. Taken together, our results demonstrate that m6A methylation modifications may play an important role in the development of NAFLD.
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spelling pubmed-86888192021-12-22 Analysis of N6-Methyladenosine Methylation Modification in Fructose-Induced Non-Alcoholic Fatty Liver Disease Luo, Yunchen Zhang, Zhijian Xiang, Liping Zhou, Bing Wang, Xuejiao Lin, Yi Ding, Xiaoying Liu, Fang Lu, Yan Peng, Yongde Front Endocrinol (Lausanne) Endocrinology Improvements in living standards have led to non-alcoholic fatty liver disease (NAFLD), one of the most common chronic liver diseases worldwide. Recent studies have shown that N6-methyladenosine (m6A), a type of RNA modification, is strongly associated with many important biological processes. However, the relationship between m6A methylation modifications and NAFLD remains poorly understood. In the present study, through methylated RNA immunoprecipitation sequencing and RNA transcriptome sequencing in high fructose diet-induced NAFLD mice, we found that hypermethylation-encoding genes were mainly enriched in lipid metabolism processes. We identified 266 overlapping and differentially expressed genes (DEGs) that changed at both the mRNA expression level and m6A modification level. Among them, 193 genes displayed increased expression and m6A modification, indicating that m6A RNA modifications tend to be positively correlated with NAFLD. We further compared the high fructose diet-induced NAFLD mouse model with leptin receptor-deficient mice and found that DEGs enriched in the lipid metabolism pathway were up-regulated in both groups. In contrast, DEGs associated with the immune inflammatory response were up-regulated in the high fructose diet group, but down-regulated in leptin receptor-deficient mice. Taken together, our results demonstrate that m6A methylation modifications may play an important role in the development of NAFLD. Frontiers Media S.A. 2021-12-07 /pmc/articles/PMC8688819/ /pubmed/34950107 http://dx.doi.org/10.3389/fendo.2021.780617 Text en Copyright © 2021 Luo, Zhang, Xiang, Zhou, Wang, Lin, Ding, Liu, Lu and Peng https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Luo, Yunchen
Zhang, Zhijian
Xiang, Liping
Zhou, Bing
Wang, Xuejiao
Lin, Yi
Ding, Xiaoying
Liu, Fang
Lu, Yan
Peng, Yongde
Analysis of N6-Methyladenosine Methylation Modification in Fructose-Induced Non-Alcoholic Fatty Liver Disease
title Analysis of N6-Methyladenosine Methylation Modification in Fructose-Induced Non-Alcoholic Fatty Liver Disease
title_full Analysis of N6-Methyladenosine Methylation Modification in Fructose-Induced Non-Alcoholic Fatty Liver Disease
title_fullStr Analysis of N6-Methyladenosine Methylation Modification in Fructose-Induced Non-Alcoholic Fatty Liver Disease
title_full_unstemmed Analysis of N6-Methyladenosine Methylation Modification in Fructose-Induced Non-Alcoholic Fatty Liver Disease
title_short Analysis of N6-Methyladenosine Methylation Modification in Fructose-Induced Non-Alcoholic Fatty Liver Disease
title_sort analysis of n6-methyladenosine methylation modification in fructose-induced non-alcoholic fatty liver disease
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8688819/
https://www.ncbi.nlm.nih.gov/pubmed/34950107
http://dx.doi.org/10.3389/fendo.2021.780617
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