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Qiongya Zhao, Linghong Ge, Kun Zhang, Haifeng Chen, Xinxin Zhan, Yue Yang, Qinglin Dang, Yi Zheng, Huaibin Zhou, Jianxin Lyu, Hezhi Fang. Assessment of mitochondrial function in metabolic dysfunction-associated fatty liver disease using obese mouse models. Zoological Research. doi: 10.24272/j.issn.2095-8137.2020.051
Citation: Qiongya Zhao, Linghong Ge, Kun Zhang, Haifeng Chen, Xinxin Zhan, Yue Yang, Qinglin Dang, Yi Zheng, Huaibin Zhou, Jianxin Lyu, Hezhi Fang. Assessment of mitochondrial function in metabolic dysfunction-associated fatty liver disease using obese mouse models. Zoological Research. doi: 10.24272/j.issn.2095-8137.2020.051

Assessment of mitochondrial function in metabolic dysfunction-associated fatty liver disease using obese mouse models

doi: 10.24272/j.issn.2095-8137.2020.051
Funds:  National Natural Science Foundation of China (Key Program: 81830071); Zhejiang Provincial Natural Science Foundation of China (LY19H040004 and Key Program: LR20H200001) ; Zhejiang Provincial Health science and Technology Plan (2015KYB238)
  • Received Date: 2020-03-11
  • Accepted Date: 2020-07-13
  • Rev Recd Date: 2020-07-08
  • Available Online: 2020-07-22
  • Metabolic dysfunction-associated fatty liver disease (MAFLD) is characterized by deregulated hepatic lipid metabolism; however, the association between MAFLD development and mitochondrial dysfunction has yet to be confirmed. Herein, we employed high-resolution respirometry, blue native polyacrylamide gel electrophoresis-based in-gel activity measurement, and immunoblot analysis to assess mitochondrial function in obesity-induced mouse models with varying degrees of MAFLD. Results show a slight significant decrease in hepatic mitochondrial respiration in some MAFLD mice compared to mice fed a standard diet. However, the activities, and levels of mitochondrial oxidative phosphorylation complexes remained unchanged during obesity-induced MAFLD progression. These results suggest that mitochondrial function, particularly oxidative phosphorylation, was mildly affected during obesity-induced MAFLD development. Moreover, transcriptome profiling of mouse and human liver tissues with varying degrees of MAFLD revealed that the decreased activation of mitochondria-related pathways was only associated with MAFLD of a high histological grade, whereas the major regulators of mitochondrial biogenesis were not altered in mice or humans during MAFLD development. Collectively, our results suggest that impaired hepatic mitochondrial function is not closely associated with obesity-induced MAFLD, and, therefore, therapeutic strategies targeting mitochondria for the treatment of MAFLD should be reconsidered.
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    沈阳化工大学材料科学与工程学院 沈阳 110142

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Assessment of mitochondrial function in metabolic dysfunction-associated fatty liver disease using obese mouse models

doi: 10.24272/j.issn.2095-8137.2020.051
Funds:  National Natural Science Foundation of China (Key Program: 81830071); Zhejiang Provincial Natural Science Foundation of China (LY19H040004 and Key Program: LR20H200001) ; Zhejiang Provincial Health science and Technology Plan (2015KYB238)

Abstract: Metabolic dysfunction-associated fatty liver disease (MAFLD) is characterized by deregulated hepatic lipid metabolism; however, the association between MAFLD development and mitochondrial dysfunction has yet to be confirmed. Herein, we employed high-resolution respirometry, blue native polyacrylamide gel electrophoresis-based in-gel activity measurement, and immunoblot analysis to assess mitochondrial function in obesity-induced mouse models with varying degrees of MAFLD. Results show a slight significant decrease in hepatic mitochondrial respiration in some MAFLD mice compared to mice fed a standard diet. However, the activities, and levels of mitochondrial oxidative phosphorylation complexes remained unchanged during obesity-induced MAFLD progression. These results suggest that mitochondrial function, particularly oxidative phosphorylation, was mildly affected during obesity-induced MAFLD development. Moreover, transcriptome profiling of mouse and human liver tissues with varying degrees of MAFLD revealed that the decreased activation of mitochondria-related pathways was only associated with MAFLD of a high histological grade, whereas the major regulators of mitochondrial biogenesis were not altered in mice or humans during MAFLD development. Collectively, our results suggest that impaired hepatic mitochondrial function is not closely associated with obesity-induced MAFLD, and, therefore, therapeutic strategies targeting mitochondria for the treatment of MAFLD should be reconsidered.

Qiongya Zhao, Linghong Ge, Kun Zhang, Haifeng Chen, Xinxin Zhan, Yue Yang, Qinglin Dang, Yi Zheng, Huaibin Zhou, Jianxin Lyu, Hezhi Fang. Assessment of mitochondrial function in metabolic dysfunction-associated fatty liver disease using obese mouse models. Zoological Research. doi: 10.24272/j.issn.2095-8137.2020.051
Citation: Qiongya Zhao, Linghong Ge, Kun Zhang, Haifeng Chen, Xinxin Zhan, Yue Yang, Qinglin Dang, Yi Zheng, Huaibin Zhou, Jianxin Lyu, Hezhi Fang. Assessment of mitochondrial function in metabolic dysfunction-associated fatty liver disease using obese mouse models. Zoological Research. doi: 10.24272/j.issn.2095-8137.2020.051

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