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Citrus maxima and tea regulate AMPK signaling pathway to retard the progress of nonalcoholic fatty liver disease
BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a chronic metabolic disease that easily induces hepatitis, cirrhosis, and even liver cancer. The long-term use of NAFLD therapeutic drugs produces toxicity and drug resistance. Therefore, it is necessary to develop high efficiency and low-toxic...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Open Academia
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9199835/ https://www.ncbi.nlm.nih.gov/pubmed/35757439 http://dx.doi.org/10.29219/fnr.v66.7652 |
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author | Wen, Shuai An, Ran Li, Zhi-Gang Lai, Zhao-Xiang Li, Dong-Li Cao, Jun-Xi Chen, Ruo-Hong Zhang, Wen-Ji Li, Qiu-Hua Lai, Xing-Fei Sun, Shi-Li Sun, Ling-Li |
author_facet | Wen, Shuai An, Ran Li, Zhi-Gang Lai, Zhao-Xiang Li, Dong-Li Cao, Jun-Xi Chen, Ruo-Hong Zhang, Wen-Ji Li, Qiu-Hua Lai, Xing-Fei Sun, Shi-Li Sun, Ling-Li |
author_sort | Wen, Shuai |
collection | PubMed |
description | BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a chronic metabolic disease that easily induces hepatitis, cirrhosis, and even liver cancer. The long-term use of NAFLD therapeutic drugs produces toxicity and drug resistance. Therefore, it is necessary to develop high efficiency and low-toxicity active ingredients to alleviate NAFLD. OBJECTIVE: This study aimed to reveal the role and mechanism of a new functional food CMT in alleviating NAFLD. RESULTS: In the ob/ob fatty liver mice models, the CMT extracts significantly inhibited the weight gain of the mice and reduced the accumulation of white fat. The anatomical and pathological results showed that CMT relieved fatty liver in mice and reduced excessive lipid deposition and inflammatory infiltration. Serological and liver biochemical indicators suggest that CMT reduced dyslipidemia and liver damage caused by fatty liver. CMT obviously activated the adenosine 5′-monophosphate-activated protein kinase (AMPK)/acetyl-coA carboxylase (ACC) and AMPK/fatty acid synthase (FAS) signaling pathways, promoted fat oxidation, and inhibited synthesis. Moreover, CMT regulated the expression of inflammatory factors to relieve hepatitis caused by NAFLD. CONCLUSION: The study explained the role and mechanism of CMT in alleviating NAFLD and suggested that the active ingredients of CMT might be beneficial in NAFLD therapy. |
format | Online Article Text |
id | pubmed-9199835 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Open Academia |
record_format | MEDLINE/PubMed |
spelling | pubmed-91998352022-06-24 Citrus maxima and tea regulate AMPK signaling pathway to retard the progress of nonalcoholic fatty liver disease Wen, Shuai An, Ran Li, Zhi-Gang Lai, Zhao-Xiang Li, Dong-Li Cao, Jun-Xi Chen, Ruo-Hong Zhang, Wen-Ji Li, Qiu-Hua Lai, Xing-Fei Sun, Shi-Li Sun, Ling-Li Food Nutr Res Original Article BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a chronic metabolic disease that easily induces hepatitis, cirrhosis, and even liver cancer. The long-term use of NAFLD therapeutic drugs produces toxicity and drug resistance. Therefore, it is necessary to develop high efficiency and low-toxicity active ingredients to alleviate NAFLD. OBJECTIVE: This study aimed to reveal the role and mechanism of a new functional food CMT in alleviating NAFLD. RESULTS: In the ob/ob fatty liver mice models, the CMT extracts significantly inhibited the weight gain of the mice and reduced the accumulation of white fat. The anatomical and pathological results showed that CMT relieved fatty liver in mice and reduced excessive lipid deposition and inflammatory infiltration. Serological and liver biochemical indicators suggest that CMT reduced dyslipidemia and liver damage caused by fatty liver. CMT obviously activated the adenosine 5′-monophosphate-activated protein kinase (AMPK)/acetyl-coA carboxylase (ACC) and AMPK/fatty acid synthase (FAS) signaling pathways, promoted fat oxidation, and inhibited synthesis. Moreover, CMT regulated the expression of inflammatory factors to relieve hepatitis caused by NAFLD. CONCLUSION: The study explained the role and mechanism of CMT in alleviating NAFLD and suggested that the active ingredients of CMT might be beneficial in NAFLD therapy. Open Academia 2022-06-10 /pmc/articles/PMC9199835/ /pubmed/35757439 http://dx.doi.org/10.29219/fnr.v66.7652 Text en © 2022 Shuai Wen et al. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material for any purpose, even commercially, provided the original work is properly cited and states its license. |
spellingShingle | Original Article Wen, Shuai An, Ran Li, Zhi-Gang Lai, Zhao-Xiang Li, Dong-Li Cao, Jun-Xi Chen, Ruo-Hong Zhang, Wen-Ji Li, Qiu-Hua Lai, Xing-Fei Sun, Shi-Li Sun, Ling-Li Citrus maxima and tea regulate AMPK signaling pathway to retard the progress of nonalcoholic fatty liver disease |
title | Citrus maxima and tea regulate AMPK signaling pathway to retard the progress of nonalcoholic fatty liver disease |
title_full | Citrus maxima and tea regulate AMPK signaling pathway to retard the progress of nonalcoholic fatty liver disease |
title_fullStr | Citrus maxima and tea regulate AMPK signaling pathway to retard the progress of nonalcoholic fatty liver disease |
title_full_unstemmed | Citrus maxima and tea regulate AMPK signaling pathway to retard the progress of nonalcoholic fatty liver disease |
title_short | Citrus maxima and tea regulate AMPK signaling pathway to retard the progress of nonalcoholic fatty liver disease |
title_sort | citrus maxima and tea regulate ampk signaling pathway to retard the progress of nonalcoholic fatty liver disease |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9199835/ https://www.ncbi.nlm.nih.gov/pubmed/35757439 http://dx.doi.org/10.29219/fnr.v66.7652 |
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