HarmLow evidencePaper 96

Exposure to Electromagnetic Fields from Mobile Phones and Fructose Consumption Coalesce to

Keywords

#mobile phone #electromagnetic fields #RF #1760 MHz #fructose #insulin resistance #AMPK #SIRT1 #UCP2 #FOXO1 #hypothalamus #liver #mitochondria #OXPHOS #oxidative stress #Wistar rats

Study snapshot

PublicationBiomedical and Environmental Sciences · 2023

Study typeanimal

Reported directionHarm

Evidence ratingLow

Abstract

Exposure to Electromagnetic Fields from Mobile Phones and Fructose Consumption Coalesce to Perturb Metabolic Regulators AMPK/SIRT1-UCP2/FOXO1 in Growing Rats Tripathi R, Banerjee SK, Nirala JP, Mathur R. Exposure to Electromagnetic Fields from Mobile Phones and Fructose Consumption Coalesce to Perturb Metabolic Regulators AMPK/SIRT1-UCP2/FOXO1 in Growing Rats[J]. Biomedical and Environmental Sciences, 2023, 36(11): 1045-1058. doi: 10.3967/bes2023.134 Abstract Objective In this study, the combined effect of two stressors, namely, electromagnetic fields (EMFs) from mobile phones and fructose consumption, on hypothalamic and hepatic master metabolic regulators of the AMPK/SIRT1-UCP2/FOXO1 pathway were elucidated to delineate the underlying molecular mechanisms of insulin resistance. Methods Weaned Wistar rats (28 days old) were divided into 4 groups: Normal, Exposure Only (ExpO), Fructose Only (FruO), and Exposure and Fructose (EF). Each group was provided standard laboratory chow ad libitum for 8 weeks. Additionally, the control groups, namely, the Normal and FruO groups, had unrestricted access to drinking water and fructose solution (15%), respectively. Furthermore, the respective treatment groups, namely, the ExpO and EF groups, received EMF exposure (1,760 MHz, 2 h/day x 8 weeks). In early adulthood, mitochondrial function, insulin receptor signaling, and oxidative stress signals in hypothalamic and hepatic tissues were assessed using western blotting and biochemical analysis. Result In the hypothalamic tissue of EF, SIRT1, FOXO 1, p-PI3K, p-AKT, Complex III, UCP2, MnSOD, and catalase expressions and OXPHOS and GSH activities were significantly decreased (P &lt; 0.05) compared to the Normal, ExpO, and FruO groups. In hepatic tissue of EF, the p-AMPKα, SIRT1, FOXO1, IRS1, p-PI3K, Complex I, II, III, IV, V, UCP2, and MnSOD expressions and the activity of OXPHOS, SOD, catalase, and GSH were significantly reduced compared to the Normal group (P &lt; 0.05). Conclusion The findings suggest that the combination of EMF exposure and fructose consumption during childhood and adolescence in Wistar rats disrupts the closely interlinked and multi-regulated crosstalk of insulin receptor signals, mitochondrial OXPHOS, and the antioxidant defense system in the hypothalamus and liver. Open access paper: besjournal.com

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 directionharm

PopulationWeaned Wistar rats (28 days old)

Sample sizeNot supplied

ExposureRF · 1760 MHz · 2 h/day for 8 weeks

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

In the exposure+fructose (EF) group, multiple hypothalamic markers (including SIRT1, FOXO1, p-PI3K, p-AKT, Complex III, UCP2, MnSOD, catalase) and OXPHOS and GSH activities were significantly decreased versus Normal, exposure-only, and fructose-only groups (P<0.05). In liver tissue of EF, several signaling, mitochondrial complex, and antioxidant markers (including p-AMPKα, SIRT1, FOXO1, IRS1, p-PI3K, Complex I–V, UCP2, MnSOD) and OXPHOS, SOD, catalase, and GSH activities were significantly reduced versus Normal (P<0.05).

Outcomes measured

Hypothalamic and hepatic AMPK/SIRT1-UCP2/FOXO1 pathway regulators
Insulin receptor signaling markers (e.g., IRS1, p-PI3K, p-AKT)
Mitochondrial function / OXPHOS complexes and activity
Oxidative stress / antioxidant defense markers (e.g., MnSOD, catalase, GSH)

Limitations

Sample size not reported in the provided abstract/metadata
Exposure metric (e.g., SAR) not reported in the provided abstract/metadata
Animal model; generalizability to humans not established in the provided abstract/metadata
Results emphasize combined exposure with fructose; effects of EMF alone are not fully detailed in the provided abstract/metadata

View raw extracted JSON

{
  "study_type": "animal",
  "exposure": {
    "band": "RF",
    "source": "mobile phone",
    "frequency_mhz": 1760,
    "sar_wkg": null,
    "duration": "2 h/day for 8 weeks"
  },
  "population": "Weaned Wistar rats (28 days old)",
  "sample_size": null,
  "outcomes": [
    "Hypothalamic and hepatic AMPK/SIRT1-UCP2/FOXO1 pathway regulators",
    "Insulin receptor signaling markers (e.g., IRS1, p-PI3K, p-AKT)",
    "Mitochondrial function / OXPHOS complexes and activity",
    "Oxidative stress / antioxidant defense markers (e.g., MnSOD, catalase, GSH)"
  ],
  "main_findings": "In the exposure+fructose (EF) group, multiple hypothalamic markers (including SIRT1, FOXO1, p-PI3K, p-AKT, Complex III, UCP2, MnSOD, catalase) and OXPHOS and GSH activities were significantly decreased versus Normal, exposure-only, and fructose-only groups (P<0.05). In liver tissue of EF, several signaling, mitochondrial complex, and antioxidant markers (including p-AMPKα, SIRT1, FOXO1, IRS1, p-PI3K, Complex I–V, UCP2, MnSOD) and OXPHOS, SOD, catalase, and GSH activities were significantly reduced versus Normal (P<0.05).",
  "effect_direction": "harm",
  "limitations": [
    "Sample size not reported in the provided abstract/metadata",
    "Exposure metric (e.g., SAR) not reported in the provided abstract/metadata",
    "Animal model; generalizability to humans not established in the provided abstract/metadata",
    "Results emphasize combined exposure with fructose; effects of EMF alone are not fully detailed in the provided abstract/metadata"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "mobile phone",
    "electromagnetic fields",
    "RF",
    "1760 MHz",
    "fructose",
    "insulin resistance",
    "AMPK",
    "SIRT1",
    "UCP2",
    "FOXO1",
    "hypothalamus",
    "liver",
    "mitochondria",
    "OXPHOS",
    "oxidative stress",
    "Wistar rats"
  ],
  "suggested_hubs": [
    {
      "slug": "rf-mobile-phones",
      "weight": 0.9,
      "reason": "RF EMF exposure from mobile phones at 1,760 MHz in an animal experiment."
    }
  ]
}

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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: 10.3967/bes2023.134
PubMed: Not supplied

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