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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

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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.

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Availability of data and material

All data generated or analyzed during the study are available within the paper. Uncropped and unmodified blot images used in the study are available as supporting information “SI”.

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Funding

This work was supported by grants from the Indian Council of Medical Research (ICMR), New Delhi. (Sanction No: 5/10/FR/13/2015-RBMH).

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Contributions

Conceptualization: Rajani Mathur. Data curation: Ruchi Tripathi. Formal analysis: Rajani Mathur and Ruchi Tripathi. Funding acquisition: Rajani Mathur. Investigation: Ruchi Tripathi. Methodology: Rajani Mathur, Sanjay Kumar Banerjee, and Jay Prakash Nirala. Project administration: Rajani Mathur and Ruchi Tripathi. Resources: Rajani Mathur. Software: Jay Prakash Nirala. Supervision: Rajani Mathur and Sanjay Kumar Banerjee. Validation: Sanjay Kumar Banerjee and Jay Prakash Nirala. Visualization: Rajani Mathur, Ruchi Tripathi. Writing—original draft preparation: Rajani Mathur and Ruchi Tripathi. Writing—review and editing: Sanjay Kumar Banerjee.

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Correspondence to Rajani Mathur.

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The funders did not have any role in the study design, data collection and analysis, and in the decision to publish, or preparation of the manuscript.

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All experimental protocols were approved by the Institutional Animal Ethics Committee, Delhi Institute of Pharmaceutical Sciences and Research, New Delhi (Protocol Number: IAEC/2014/II-04 and DIPSAR/IAEC/2015-II/07).

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The authors declare no competing interests.

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Tripathi, ., Banerjee, S.K., Nirala, J.P. et al. 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 29, 7438–7451 (2022). https://doi.org/10.1007/s11356-021-15841-y

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  • DOI: https://doi.org/10.1007/s11356-021-15841-y

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