Simultaneous exposure to electromagnetic field from mobile phone and unimpeded fructose drinking during pre-, peri-, and post-pubertal stages perturbs the hypothalamic and hepatic regulation of energy homeostasis by early adulthood: experimental evidence

Environmental science and pollution research international · 2021 · Harm · Low evidence

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HarmLow evidencePaper 1057

In rats, combined mobile-phone EMF exposure (2 h/day for 8 weeks) plus 15% fructose drinking solution (EF group) was associated by early adulthood with higher total calorie consumption and increased weight gain versus normal, alongside raised ghrelin. EF also…

Study snapshot

PublicationEnvironmental science and pollution research international · 2021
Study typeanimal
Reported directionHarm
Evidence ratingLow

Abstract

Simultaneous exposure to electromagnetic field from mobile phone and unimpeded fructose drinking during pre-, peri-, and post-pubertal stages perturbs the hypothalamic and hepatic regulation of energy homeostasis by early adulthood: experimental evidence Ruchi Tripathi, Sanjay Kumar Banerjee, Jay Prakash Nirala, Rajani Mathur. Simultaneous exposure to electromagnetic field from mobile phone and unimpeded fructose drinking during pre-, peri-, and post-pubertal stages perturbs the hypothalamic and hepatic regulation of energy homeostasis by early adulthood: experimental evidence. Environ Sci Pollut Res Int. 2021 Sep 2. doi: 10.1007/s11356-021-15841-y. Abstract The present-day children-adolescents ubiquitously use the mobile phones and unrestrictedly consume fructose- laden diet. Unfortunately, a rise in the incidence of insulin resistance and fatty liver syndrome in young adults has also been recorded. To delineate a possible correlate, the effect of exposure to electromagnetic field (EMF) from the mobile phone and unrestricted fructose intake during pre-, peri-, and post-pubertal stages of development on orexigenic and anorexigenic signals arising from the hypothalamus and liver of rats is investigated here. The study design included four arms, i.e., "Normal", "Exposure Only (ExpO)", "Fructose Only (FruO)", and "Exposure with Fructose (EF)", wherein weaned rats received either "normal chow and drinking water" or "normal chow and fructose (15%) drinking solution" in presence and absence of EMF exposure (2 h/day) for 8 weeks. The results indicate that the total calories consumed by the EF were higher by early adulthood than normal, possibly under the influence of the raised levels of the orexigenic hormone, i.e., ghrelin, and it reflected as raised rate of weight gain. At early adulthood, the EF recorded mitigated response and sensitivity of insulin. Despite EF being a "fed-state", both centrally and peripherally, the glycolysis was restrained, but the gluconeogenesis was raised. Additionally, the altered lipid profile and the glycogen levels indicate that the EF developed fatty liver. The energy homeostasis of the EF was compromised as evidenced by (a) reduced expression of the glucosensors-GLUT2 and glucokinase in the hypothalamus and liver and (b) reduced expression of the cellular energy regulator-AMPK, orexigenic peptide-NPY, and anorexigenic peptide- POMC in the hypothalamus. Taken together, the present study evidences that the exposure to EMFfrom the mobile phone and unrestricted fructose intake during childhood-adolescence impairs the central and peripheral pathways that mediate the glucosensing, glucoregulation, feeding, and satiety behavior by early adulthood. pubmed.ncbi.nlm.nih.gov

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 rats (pre-, peri-, and post-pubertal developmental stages; assessed by early adulthood)
Sample sizeNot supplied
Exposure2 h/day for 8 weeks (during pre-, peri-, and post-pubertal stages)
Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

In rats, combined mobile-phone EMF exposure (2 h/day for 8 weeks) plus 15% fructose drinking solution (EF group) was associated by early adulthood with higher total calorie consumption and increased weight gain versus normal, alongside raised ghrelin. EF also showed mitigated insulin response/sensitivity, restrained glycolysis with raised gluconeogenesis despite a fed state, altered lipid profile and glycogen levels consistent with fatty liver, and reduced hypothalamic and hepatic expression of GLUT2 and glucokinase; hypothalamic AMPK, NPY, and POMC expression were also reduced.

Outcomes measured

  • Caloric intake
  • Ghrelin (orexigenic hormone)
  • Weight gain
  • Insulin response/sensitivity
  • Glycolysis
  • Gluconeogenesis
  • Lipid profile
  • Glycogen levels
  • Fatty liver development
  • Hypothalamic and hepatic expression of GLUT2
  • Hypothalamic and hepatic expression of glucokinase
  • Hypothalamic expression of AMPK
  • Hypothalamic expression of NPY
  • Hypothalamic expression of POMC
  • Energy homeostasis/glucosensing/glucoregulation/feeding and satiety pathways

Limitations

  • Frequency and SAR of the mobile-phone EMF exposure not reported in the abstract
  • Sample size not reported in the abstract
  • Animal model; generalizability to humans not established in the abstract
  • Exposure-only and fructose-only arm results are not detailed in the abstract, limiting attribution of effects to EMF vs fructose vs interaction
View raw extracted JSON
{
  "study_type": "animal",
  "exposure": {
    "band": null,
    "source": "mobile phone",
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": "2 h/day for 8 weeks (during pre-, peri-, and post-pubertal stages)"
  },
  "population": "Weaned rats (pre-, peri-, and post-pubertal developmental stages; assessed by early adulthood)",
  "sample_size": null,
  "outcomes": [
    "Caloric intake",
    "Ghrelin (orexigenic hormone)",
    "Weight gain",
    "Insulin response/sensitivity",
    "Glycolysis",
    "Gluconeogenesis",
    "Lipid profile",
    "Glycogen levels",
    "Fatty liver development",
    "Hypothalamic and hepatic expression of GLUT2",
    "Hypothalamic and hepatic expression of glucokinase",
    "Hypothalamic expression of AMPK",
    "Hypothalamic expression of NPY",
    "Hypothalamic expression of POMC",
    "Energy homeostasis/glucosensing/glucoregulation/feeding and satiety pathways"
  ],
  "main_findings": "In rats, combined mobile-phone EMF exposure (2 h/day for 8 weeks) plus 15% fructose drinking solution (EF group) was associated by early adulthood with higher total calorie consumption and increased weight gain versus normal, alongside raised ghrelin. EF also showed mitigated insulin response/sensitivity, restrained glycolysis with raised gluconeogenesis despite a fed state, altered lipid profile and glycogen levels consistent with fatty liver, and reduced hypothalamic and hepatic expression of GLUT2 and glucokinase; hypothalamic AMPK, NPY, and POMC expression were also reduced.",
  "effect_direction": "harm",
  "limitations": [
    "Frequency and SAR of the mobile-phone EMF exposure not reported in the abstract",
    "Sample size not reported in the abstract",
    "Animal model; generalizability to humans not established in the abstract",
    "Exposure-only and fructose-only arm results are not detailed in the abstract, limiting attribution of effects to EMF vs fructose vs interaction"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "mobile phone",
    "electromagnetic field",
    "fructose",
    "puberty",
    "rats",
    "hypothalamus",
    "liver",
    "energy homeostasis",
    "insulin resistance",
    "fatty liver",
    "ghrelin",
    "GLUT2",
    "glucokinase",
    "AMPK",
    "NPY",
    "POMC"
  ],
  "suggested_hubs": [
    {
      "slug": "mobile-phones-rf",
      "weight": 0.9,
      "reason": "Study investigates EMF exposure from mobile phone."
    }
  ]
}
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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: 10.1007/s11356-021-15841-y
PubMed: 34476698

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