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

PAPER pubmed Biomedical engineering online 2023 Animal study Effect: benefit Evidence: Low

Read original paper → DOI: 10.1186/s12938-023-01114-x PMID: 37217972 Evidence Lab

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.

AI evidence extraction

At a glance

Study type

Animal study

Effect direction

benefit

Population

Mice with NAFLD induced by high-fat diet (HFD-fed mice)

Sample size

—

Exposure

Evidence strength

Low

Confidence: 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": 0.7399999999999999911182158029987476766109466552734375,
    "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/metadata and may be incomplete or incorrect. This content is for informational purposes only and is not medical advice.

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