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Background <p>Metabolic associated steatotic liver disease (MASLD), characterized by mitochondrial dysfunction. It may be ameliorated by electroacupuncture (EA) through activation of the ten-eleven translocation 1 (TET1)/peroxisome proliferator-activated receptor-α (PPARα) pathway, thereby restoring mitochondrial function.</p> Methods <p>C57BL/6 mice were fed L-amino acid rodent diet with 60&#xa0;kcal% fat, low methionine and no added choline (CDAHFD) and high fat diet (HFD) for three weeks to induce MASLD, followed by EA treatment and daily intraperitoneal injections of a TET1 agonist or antagonist. Hepatic lipid accumulation, inflammatory cytokines, reactive oxygen species (ROS), and mitochondrial function were evaluated by biochemical assays, enzyme-linked immunosorbent assay (ELISA), flow cytometry, and transmission electron microscopy (TEM), western blotting (WB) and reverse transcription quantitative polymerase chain reaction (RT-qPCR).</p> Results <p>EA reduced hepatic total cholesterol (TC), triglycerides (TG), and free fatty acids (FFA), and decreased the size of lipid droplets. It restored mitochondrial membrane potential, ATP production, and cristae integrity, while attenuating ROS accumulation and suppressing pro-inflammatory cytokine levels. Moreover, EA upregulated TET1 expression, enhanced genomic 5-hydroxymethylcytosine (5-hmC) enrichment, and elevated PPARα expression. These effects were comparable to those of a TET1 agonist, whereas administration of a TET1 antagonist partially reversed them.</p> Conclusion <p>EA ameliorates MASLD by activating the TET1/PPARα pathway, thereby enhancing mitochondrial function and reducing oxidative stress and inflammation.</p> Clinical trial number <p>Not applicable.</p>

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Electroacupuncture activates the TET1/PPARα pathway to protect mitochondrial function in MASLD

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月2日

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  • Shurui Yang,
  • Yiwen Li,
  • Bowen Lu,
  • Congcong Cheng,
  • Yayuan Wang,
  • Li Chen

摘要

Background

Metabolic associated steatotic liver disease (MASLD), characterized by mitochondrial dysfunction. It may be ameliorated by electroacupuncture (EA) through activation of the ten-eleven translocation 1 (TET1)/peroxisome proliferator-activated receptor-α (PPARα) pathway, thereby restoring mitochondrial function.

Methods

C57BL/6 mice were fed L-amino acid rodent diet with 60 kcal% fat, low methionine and no added choline (CDAHFD) and high fat diet (HFD) for three weeks to induce MASLD, followed by EA treatment and daily intraperitoneal injections of a TET1 agonist or antagonist. Hepatic lipid accumulation, inflammatory cytokines, reactive oxygen species (ROS), and mitochondrial function were evaluated by biochemical assays, enzyme-linked immunosorbent assay (ELISA), flow cytometry, and transmission electron microscopy (TEM), western blotting (WB) and reverse transcription quantitative polymerase chain reaction (RT-qPCR).

Results

EA reduced hepatic total cholesterol (TC), triglycerides (TG), and free fatty acids (FFA), and decreased the size of lipid droplets. It restored mitochondrial membrane potential, ATP production, and cristae integrity, while attenuating ROS accumulation and suppressing pro-inflammatory cytokine levels. Moreover, EA upregulated TET1 expression, enhanced genomic 5-hydroxymethylcytosine (5-hmC) enrichment, and elevated PPARα expression. These effects were comparable to those of a TET1 agonist, whereas administration of a TET1 antagonist partially reversed them.

Conclusion

EA ameliorates MASLD by activating the TET1/PPARα pathway, thereby enhancing mitochondrial function and reducing oxidative stress and inflammation.

Clinical trial number

Not applicable.