Evidence map›Paper›PMID 36224316›Full record

ArticleBiological trace element research2023

Magnesium Supplementation Stimulates Autophagy to Reduce Lipid Accumulation in Hepatocytes via the AMPK/mTOR Pathway.

Shiyan Chen, Shunkui Luo, Baojia Zou, Jianhui Xie, Jian Li, Yingjuan Zeng

Abstract read
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In one paragraph

Article in Biological trace element research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

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  6. Zinc Depletion Increases Susceptibility to AMPK-Induced Atrophic Responses in C2C12 Myotubes.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Shiyan Chen *Department of Endocrinology and Metabolic Diseases, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China.
Shunkui Luo *Department of Endocrinology and Metabolic Diseases, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China.
Baojia ZouDepartment of Hepatobiliary Surgery, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China.
Jianhui XieDepartment of Endocrinology and Metabolic Diseases, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China.
Jian LiDepartment of Hepatobiliary Surgery, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China. lijian5@mail.sysu.edu.cn.
Yingjuan ZengDepartment of Endocrinology and Metabolic Diseases, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China. zyingj@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-0851-4212
Sun Yat-sen University · CN

Funding

Medical Science and Technology Foundation of Guangdong Province No. A2022347National Natural Science Foundation of China No. 81700716Natural Science Foundation of Guangdong Province No. 2022A1515011244Science and Technology Planning Project in the field of social development of Zhuhai of Guangdong Province No. 2220004000269
6 · The paper itself

Abstract

Metabolic-associated fatty liver disease (MAFLD) (previously known as nonalcoholic fatty liver disease (NAFLD)) is a disease with high worldwide prevalence, but with limited available therapeutic interventions. Autophagy is a cell survival mechanism for clearing excess lipids in hepatocytes and affects the occurrence and development of MAFLD. In addition, some studies have shown that magnesium deficiency is common in patients with obesity and metabolic syndrome. Magnesium supplementation can effectively improve metabolism-related diseases such as obesity and fatty liver. Our study successfully constructed a cellular model of MAFLD by 1 mM free fatty acid (FFA) intervention in LO2 cells for 24 h, and there was an increase in lipid accumulation in hepatocytes after FFA intervention. Magnesium supplementation was shown to reduce lipid deposition in hepatocytes induced by FFA, and Western blotting (WB) analysis showed that magnesium supplementation could downregulate the expression of Fasn and SREBP1 and increase the expression of LPL, suggesting that magnesium can reduce lipid accumulation by reducing lipid synthesis and increasing lipid oxidation. Magnesium supplementation could affect cellular lipid metabolism by activating the AMPK/mTOR pathway to stimulate autophagy. Our results identified a relationship between magnesium and lipid accumulation in hepatocytes and showed that magnesium supplementation reduced lipid deposition in hepatocytes by activating autophagy by activating the AMPK-mTOR pathway.

Indexed as

LiverNon-alcoholic Fatty Liver DiseaseAMP-Activated Protein KinasesAutophagyDietary SupplementsFatty Acids, NonesterifiedHepatocytesHumansLipid MetabolismMagnesiumObesitySignal TransductionTOR Serine-Threonine KinasesAMP-Activated Protein KinasesFatty Acids, NonesterifiedMagnesiumMTOR protein, humanTOR Serine-Threonine KinasesAutophagyLipid metabolismMagnesiumMetabolic-associated fatty liver disease

Identifiers

PMID36224316
OpenAlexW4304756684

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.