Liver knockout of MCU leads to greater dysregulation of lipid metabolism in MAFLD

Metabolic-associated fatty liver disease (MAFLD) is a common chronic condition that poses a significant threat to human health. Mitochondrial dysfunction, particularly involving the mitochondrial Ca<sup>2+</sup> uniporter (MCU), plays a key role in its pathogenesis. This study aimed to investigate the impact of the MCU gene on hepatic lipid metabolism in mice fed a high-fat diet. Using MCU knockout and wild-type mice, subjected to either a high-fat or normal diet for 14 weeks, we observed notable Steatosis and liver weight gain in MCU-deficient mice. Liver function markers, serum triglycerides, very low-density lipoprotein (VLDL) levels, and ApoB protein expression were all significantly elevated. Mechanistic studies revealed that MCU deletion led to mitochondrial dysfunction, increased oxidative stress. These findings highlight the critical role of the MCU gene in maintaining hepatic lipid balance and suggest its potential as a therapeutic target for managing nonalcoholic fatty liver disease.

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Publication Details

Journal
Scientific Reports
Published
2024-11-15
DOI
https://doi.org/10.1038/s41598-024-78935-w
Citations
3
Primary Topic
Liver Disease Diagnosis and Treatment
Type
article
Field-Weighted Citation Impact
1.16

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article

Liver knockout of MCU leads to greater dysregulation of lipid metabolism in MAFLD

Turtushikh Damba, Xinyi Qi, Tingli Pan, Zhiwang Zhang et al.
3 citations
Scientific Reports
Liver Disease Diagnosis and Treatment
1.16
article

Liver knockout of MCU leads to greater dysregulation of lipid metabolism in MAFLD

Turtushikh Damba, Xinyi Qi, Tingli Pan, Zhiwang Zhang, Xinyu Qi, Lin Yu, Yun‐Xiao Liang, Yurou Zhang, Tianyu Jiang, Songtao Su, Suosu Wei, Qichao Liao, Khongorzul Batchuluun, Xiangling Li, Lei Zhou, Siqi Liu, Yixing Li, Liu Shi, Zupeng Luo, Yang Xiao, Yu Sun
article en
3 citations

Abstract

Metabolic-associated fatty liver disease (MAFLD) is a common chronic condition that poses a significant threat to human health. Mitochondrial dysfunction, particularly involving the mitochondrial Ca<sup>2+</sup> uniporter (MCU), plays a key role in its pathogenesis. This study aimed to investigate the impact of the MCU gene on hepatic lipid metabolism in mice fed a high-fat diet. Using MCU knockout and wild-type mice, subjected to either a high-fat or normal diet for 14 weeks, we observed notable Steatosis and liver weight gain in MCU-deficient mice. Liver function markers, serum triglycerides, very low-density lipoprotein (VLDL) levels, and ApoB protein expression were all significantly elevated. Mechanistic studies revealed that MCU deletion led to mitochondrial dysfunction, increased oxidative stress. These findings highlight the critical role of the MCU gene in maintaining hepatic lipid balance and suggest its potential as a therapeutic target for managing nonalcoholic fatty liver disease.

Scientific ReportsVol. 14(1)
Guangxi University (CN), Mongolian National University of Medical Sciences (MN), The People's Hospital of Guangxi Zhuang Autonomous Region (CN)
Deutsches Krebsforschungszentrum, National Natural Science Foundation of China, National Key Research and Development Program of China
Zero hunger
Openalex Percentile: Top 19%
Liver Disease Diagnosis and Treatment
1.16
DOIOpen Access PDFOpenAlex
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