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Maca extracts regulate glucose and lipid metabolism in insulin‐resistant HepG2 cells via the PI3K/AKT signalling pathway

This work focused on the separation of the active ingredients of maca (Lepidium meyenii Walpers) and evaluated the antioxidative capability of these components with effects on improving glucose and lipid metabolism in insulin‐resistant HepG2 cells. DPPH free radical scavenging and reducing power ass...

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Detalles Bibliográficos
Autores principales: Li, Aimin, Liu, Jia, Ding, Fangli, Wu, Xiaolei, Pan, Cong, Wang, Qing, Gao, Ming, Duan, Shenglin, Han, Xiaofeng, Xia, Kai, Liu, Shiwei, Wu, Yimin, Zhou, Zhiqiao, Zhang, Xi, Gao, Xiao‐Dong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8194906/
https://www.ncbi.nlm.nih.gov/pubmed/34136157
http://dx.doi.org/10.1002/fsn3.2246
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author Li, Aimin
Liu, Jia
Ding, Fangli
Wu, Xiaolei
Pan, Cong
Wang, Qing
Gao, Ming
Duan, Shenglin
Han, Xiaofeng
Xia, Kai
Liu, Shiwei
Wu, Yimin
Zhou, Zhiqiao
Zhang, Xi
Gao, Xiao‐Dong
author_facet Li, Aimin
Liu, Jia
Ding, Fangli
Wu, Xiaolei
Pan, Cong
Wang, Qing
Gao, Ming
Duan, Shenglin
Han, Xiaofeng
Xia, Kai
Liu, Shiwei
Wu, Yimin
Zhou, Zhiqiao
Zhang, Xi
Gao, Xiao‐Dong
author_sort Li, Aimin
collection PubMed
description This work focused on the separation of the active ingredients of maca (Lepidium meyenii Walpers) and evaluated the antioxidative capability of these components with effects on improving glucose and lipid metabolism in insulin‐resistant HepG2 cells. DPPH free radical scavenging and reducing power assays were used to evaluate the antioxidant activity of maca extracts. An insulin‐resistant HepG2 cell model induced by glucose, fructose, oleic acid, and palmitic acid was adopted to investigate the effects of maca extracts on regulating glucose and lipid metabolism in this study. LC‐MS/MS was then used for determination of the maca n‐butanol (NBT) subfraction. The results showed that maca ethanol extract and subfractions of this extract exhibited certain antioxidant capacity. Furthermore, the NBT subfraction reversed the disorders in glucose and lipid metabolism in insulin‐resistant HepG2 cells and significantly increased the mRNA expression of phosphoinositide 3‐kinases (PI3K) and AKT in insulin‐resistant HepG2 cells in a dose‐dependent manner. In addition, the LC‐MS/MS results showed that the NBT subfraction contained many active ingredients. Overall, this study suggests that the NBT subfraction of the ethanol extract rich in glucosinolates modulates insulin resistance via PI3K/AKT activation in insulin‐resistant HepG2 cells and might exert potentially beneficial effects in improving or treating glucose and lipid metabolic disorders.
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spelling pubmed-81949062021-06-15 Maca extracts regulate glucose and lipid metabolism in insulin‐resistant HepG2 cells via the PI3K/AKT signalling pathway Li, Aimin Liu, Jia Ding, Fangli Wu, Xiaolei Pan, Cong Wang, Qing Gao, Ming Duan, Shenglin Han, Xiaofeng Xia, Kai Liu, Shiwei Wu, Yimin Zhou, Zhiqiao Zhang, Xi Gao, Xiao‐Dong Food Sci Nutr Original Research This work focused on the separation of the active ingredients of maca (Lepidium meyenii Walpers) and evaluated the antioxidative capability of these components with effects on improving glucose and lipid metabolism in insulin‐resistant HepG2 cells. DPPH free radical scavenging and reducing power assays were used to evaluate the antioxidant activity of maca extracts. An insulin‐resistant HepG2 cell model induced by glucose, fructose, oleic acid, and palmitic acid was adopted to investigate the effects of maca extracts on regulating glucose and lipid metabolism in this study. LC‐MS/MS was then used for determination of the maca n‐butanol (NBT) subfraction. The results showed that maca ethanol extract and subfractions of this extract exhibited certain antioxidant capacity. Furthermore, the NBT subfraction reversed the disorders in glucose and lipid metabolism in insulin‐resistant HepG2 cells and significantly increased the mRNA expression of phosphoinositide 3‐kinases (PI3K) and AKT in insulin‐resistant HepG2 cells in a dose‐dependent manner. In addition, the LC‐MS/MS results showed that the NBT subfraction contained many active ingredients. Overall, this study suggests that the NBT subfraction of the ethanol extract rich in glucosinolates modulates insulin resistance via PI3K/AKT activation in insulin‐resistant HepG2 cells and might exert potentially beneficial effects in improving or treating glucose and lipid metabolic disorders. John Wiley and Sons Inc. 2021-03-29 /pmc/articles/PMC8194906/ /pubmed/34136157 http://dx.doi.org/10.1002/fsn3.2246 Text en © 2021 The Authors. Food Science & Nutrition published by Wiley Periodicals LLC https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Li, Aimin
Liu, Jia
Ding, Fangli
Wu, Xiaolei
Pan, Cong
Wang, Qing
Gao, Ming
Duan, Shenglin
Han, Xiaofeng
Xia, Kai
Liu, Shiwei
Wu, Yimin
Zhou, Zhiqiao
Zhang, Xi
Gao, Xiao‐Dong
Maca extracts regulate glucose and lipid metabolism in insulin‐resistant HepG2 cells via the PI3K/AKT signalling pathway
title Maca extracts regulate glucose and lipid metabolism in insulin‐resistant HepG2 cells via the PI3K/AKT signalling pathway
title_full Maca extracts regulate glucose and lipid metabolism in insulin‐resistant HepG2 cells via the PI3K/AKT signalling pathway
title_fullStr Maca extracts regulate glucose and lipid metabolism in insulin‐resistant HepG2 cells via the PI3K/AKT signalling pathway
title_full_unstemmed Maca extracts regulate glucose and lipid metabolism in insulin‐resistant HepG2 cells via the PI3K/AKT signalling pathway
title_short Maca extracts regulate glucose and lipid metabolism in insulin‐resistant HepG2 cells via the PI3K/AKT signalling pathway
title_sort maca extracts regulate glucose and lipid metabolism in insulin‐resistant hepg2 cells via the pi3k/akt signalling pathway
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8194906/
https://www.ncbi.nlm.nih.gov/pubmed/34136157
http://dx.doi.org/10.1002/fsn3.2246
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