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Electromagnetic fields ameliorate hepatic lipid accumulation and oxidative stress: potential role of CaMKKβ/AMPK/SREBP-1c and Nrf2 pathways.

Biomedical engineering online · 2023 · Benefit · Low evidence

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BenefitLow evidencePaper 5792

In HFD-fed mice, EMF exposure decreased body weight, liver weight, and serum TG levels and reduced excessive hepatic lipid accumulation. EMF increased CaMKKβ protein expression, activated AMPK phosphorylation, suppressed mature SREBP-1c, and increased nuclear…

Study snapshot

PublicationBiomedical engineering online · 2023
Study typeanimal
Reported directionBenefit
Evidence ratingLow

Abstract

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide, and is related to disturbed lipid metabolism and redox homeostasis. However, a definitive drug treatment has not been approved for this disease. Studies have found that electromagnetic fields (EMF) can ameliorate hepatic steatosis and oxidative stress. Nevertheless, the mechanism remains unclear. METHODS: NAFLD models were established by feeding mice a high-fat diet. Simultaneously, EMF exposure is performed. The effects of the EMF on hepatic lipid deposition and oxidative stress were investigated. Additionally, the AMPK and Nrf2 pathways were analysed to confirm whether they were activated by the EMF. RESULTS: Exposure to EMF decreased the body weight, liver weight and serum triglyceride (TG) levels and restrained the excessive hepatic lipid accumulation caused by feeding the HFD. The EMF boosted CaMKKβ protein expression, activated AMPK phosphorylation and suppressed mature SREBP-1c protein expression. Meanwhile, the activity of GSH-Px was enhanced following an increase in nuclear Nrf2 protein expression by PEMF. However, no change was observed in the activities of SOD and CAT. Consequently, EMF reduced hepatic reactive oxygen species (ROS) and MDA levels, which means that EMF relieved liver damage caused by oxidative stress in HFD-fed mice. CONCLUSIONS: EMF may activate the CaMKKβ/AMPK/SREBP-1c and Nrf2 pathways to control hepatic lipid deposition and oxidative stress. This investigation indicates that EMF may be a novel therapeutic method for NAFLD.

Machine Enhanced Logic

AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typeanimal
Effect directionbenefit
PopulationMice with NAFLD induced by high-fat diet (HFD-fed mice)
Sample sizeNot supplied
ExposureNot supplied
Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

In HFD-fed mice, EMF exposure decreased body weight, liver weight, and serum TG levels and reduced excessive hepatic lipid accumulation. EMF increased CaMKKβ protein expression, activated AMPK phosphorylation, suppressed mature SREBP-1c, and increased nuclear Nrf2 with enhanced GSH-Px activity; SOD and CAT activities did not change. EMF exposure reduced hepatic ROS and MDA levels, consistent with reduced oxidative stress-related liver damage.

Outcomes measured

  • Body weight
  • Liver weight
  • Serum triglyceride (TG) levels
  • Hepatic lipid accumulation/steatosis
  • CaMKKβ protein expression
  • AMPK phosphorylation
  • Mature SREBP-1c protein expression
  • Nuclear Nrf2 protein expression
  • GSH-Px activity
  • SOD activity
  • CAT activity
  • Hepatic reactive oxygen species (ROS)
  • Malondialdehyde (MDA) levels
  • Oxidative stress-related liver damage

Limitations

  • EMF exposure parameters (e.g., frequency, intensity, duration, SAR) not provided in the abstract
  • Animal model (mice) limits direct generalization to humans
  • Sample size not reported in the abstract
View raw extracted JSON
{
  "study_type": "animal",
  "exposure": {
    "band": null,
    "source": null,
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Mice with NAFLD induced by high-fat diet (HFD-fed mice)",
  "sample_size": null,
  "outcomes": [
    "Body weight",
    "Liver weight",
    "Serum triglyceride (TG) levels",
    "Hepatic lipid accumulation/steatosis",
    "CaMKKβ protein expression",
    "AMPK phosphorylation",
    "Mature SREBP-1c protein expression",
    "Nuclear Nrf2 protein expression",
    "GSH-Px activity",
    "SOD activity",
    "CAT activity",
    "Hepatic reactive oxygen species (ROS)",
    "Malondialdehyde (MDA) levels",
    "Oxidative stress-related liver damage"
  ],
  "main_findings": "In HFD-fed mice, EMF exposure decreased body weight, liver weight, and serum TG levels and reduced excessive hepatic lipid accumulation. EMF increased CaMKKβ protein expression, activated AMPK phosphorylation, suppressed mature SREBP-1c, and increased nuclear Nrf2 with enhanced GSH-Px activity; SOD and CAT activities did not change. EMF exposure reduced hepatic ROS and MDA levels, consistent with reduced oxidative stress-related liver damage.",
  "effect_direction": "benefit",
  "limitations": [
    "EMF exposure parameters (e.g., frequency, intensity, duration, SAR) not provided in the abstract",
    "Animal model (mice) limits direct generalization to humans",
    "Sample size not reported in the abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "electromagnetic fields",
    "EMF",
    "PEMF",
    "nonalcoholic fatty liver disease",
    "NAFLD",
    "high-fat diet",
    "hepatic steatosis",
    "oxidative stress",
    "CaMKKβ",
    "AMPK",
    "SREBP-1c",
    "Nrf2",
    "GSH-Px",
    "ROS",
    "MDA"
  ],
  "suggested_hubs": []
}
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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1186/s12938-023-01114-x
PubMed: 37217972

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