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Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK

BACKGROUND AND AIMS: Lipid accumulation is the major characteristic of non-alcoholic fatty liver disease, the prevalence of which continues to rise. We aimed to investigate the effects and mechanisms of icaritin on lipid accumulation. METHODS: Cells were treated with icaritin at 0.7, 2.2, 6.7, or 20...

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Autores principales: Wu, Yue, Yang, Ying, Li, Fang, Zou, Jie, Wang, Yu-Hao, Xu, Meng-Xia, Wang, Yong-Lun, Li, Rui-Xi, Sun, Yu-Ting, Lu, Shun, Zhang, Yuan-Yuan, Sun, Xiao-Dong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: XIA & HE Publishing Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8237137/
https://www.ncbi.nlm.nih.gov/pubmed/34221923
http://dx.doi.org/10.14218/JCTH.2021.00050
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author Wu, Yue
Yang, Ying
Li, Fang
Zou, Jie
Wang, Yu-Hao
Xu, Meng-Xia
Wang, Yong-Lun
Li, Rui-Xi
Sun, Yu-Ting
Lu, Shun
Zhang, Yuan-Yuan
Sun, Xiao-Dong
author_facet Wu, Yue
Yang, Ying
Li, Fang
Zou, Jie
Wang, Yu-Hao
Xu, Meng-Xia
Wang, Yong-Lun
Li, Rui-Xi
Sun, Yu-Ting
Lu, Shun
Zhang, Yuan-Yuan
Sun, Xiao-Dong
author_sort Wu, Yue
collection PubMed
description BACKGROUND AND AIMS: Lipid accumulation is the major characteristic of non-alcoholic fatty liver disease, the prevalence of which continues to rise. We aimed to investigate the effects and mechanisms of icaritin on lipid accumulation. METHODS: Cells were treated with icaritin at 0.7, 2.2, 6.7, or 20 µM for 24 h. The effects on lipid accumulation in L02 and Huh-7 cells were detected by Bodipy and oil red O staining, respectively. Mitochondria biogenesis of L02 cells was detected by MitoTracker Orange staining. Glucose uptake and adenosine triphosphate content of 3T3-L1 adipocytes and C2C12 myotubes were detected. The expression levels of proteins in the adenosine 5′-monophosphate-activated protein kinase (AMPK) signaling pathway, biomarkers of autophagy, and mitochondria biogenesis were measured by western blotting. LC3 puncta were detected by immunofluorescence. RESULTS: Icaritin significantly attenuated lipid accumulation in L02 and Huh-7 cells and boosted the mitochondria biogenesis of L02 cells. Icaritin enhanced glucose uptake, decreased adenosine triphosphate content, and activated the AMPK signaling pathway in 3T3-L1 adipocytes and C2C12 myotubes. Icaritin boosted autophagy and also enhanced the initiation of autophagic flux in 3T3-L1 preadipocytes and C2C12 myoblasts. However, icaritin decreased autophagy and promoted mitochondria biogenesis in 3T3-L1 adipocytes and C2C12 myotubes. CONCLUSIONS: Icaritin attenuates lipid accumulation by increasing energy expenditure and regulating autophagy by activating the AMPK pathway.
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spelling pubmed-82371372021-07-01 Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK Wu, Yue Yang, Ying Li, Fang Zou, Jie Wang, Yu-Hao Xu, Meng-Xia Wang, Yong-Lun Li, Rui-Xi Sun, Yu-Ting Lu, Shun Zhang, Yuan-Yuan Sun, Xiao-Dong J Clin Transl Hepatol Original Article BACKGROUND AND AIMS: Lipid accumulation is the major characteristic of non-alcoholic fatty liver disease, the prevalence of which continues to rise. We aimed to investigate the effects and mechanisms of icaritin on lipid accumulation. METHODS: Cells were treated with icaritin at 0.7, 2.2, 6.7, or 20 µM for 24 h. The effects on lipid accumulation in L02 and Huh-7 cells were detected by Bodipy and oil red O staining, respectively. Mitochondria biogenesis of L02 cells was detected by MitoTracker Orange staining. Glucose uptake and adenosine triphosphate content of 3T3-L1 adipocytes and C2C12 myotubes were detected. The expression levels of proteins in the adenosine 5′-monophosphate-activated protein kinase (AMPK) signaling pathway, biomarkers of autophagy, and mitochondria biogenesis were measured by western blotting. LC3 puncta were detected by immunofluorescence. RESULTS: Icaritin significantly attenuated lipid accumulation in L02 and Huh-7 cells and boosted the mitochondria biogenesis of L02 cells. Icaritin enhanced glucose uptake, decreased adenosine triphosphate content, and activated the AMPK signaling pathway in 3T3-L1 adipocytes and C2C12 myotubes. Icaritin boosted autophagy and also enhanced the initiation of autophagic flux in 3T3-L1 preadipocytes and C2C12 myoblasts. However, icaritin decreased autophagy and promoted mitochondria biogenesis in 3T3-L1 adipocytes and C2C12 myotubes. CONCLUSIONS: Icaritin attenuates lipid accumulation by increasing energy expenditure and regulating autophagy by activating the AMPK pathway. XIA & HE Publishing Inc. 2021-06-28 2021-03-08 /pmc/articles/PMC8237137/ /pubmed/34221923 http://dx.doi.org/10.14218/JCTH.2021.00050 Text en © 2021 Authors. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 4.0 International License (CC BY-NC 4.0), permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Wu, Yue
Yang, Ying
Li, Fang
Zou, Jie
Wang, Yu-Hao
Xu, Meng-Xia
Wang, Yong-Lun
Li, Rui-Xi
Sun, Yu-Ting
Lu, Shun
Zhang, Yuan-Yuan
Sun, Xiao-Dong
Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK
title Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK
title_full Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK
title_fullStr Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK
title_full_unstemmed Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK
title_short Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK
title_sort icaritin attenuates lipid accumulation by increasing energy expenditure and autophagy regulated by phosphorylating ampk
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8237137/
https://www.ncbi.nlm.nih.gov/pubmed/34221923
http://dx.doi.org/10.14218/JCTH.2021.00050
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