Exposure to Electromagnetic Fields from Mobile Phones and Fructose consumption Coalesce to Perturb Metabolic Regulators AMPK/SIRT1-UCP2/FOXO1 in Growing Rats.

Ruchi Tripathi; Sanjay Kumar Banerjee; Jay Prakash Nirala; Rajani Mathur

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Exposure to Electromagnetic Fields from Mobile Phones and Fructose consumption Coalesce to Perturb Metabolic Regulators AMPK/SIRT1-UCP2/FOXO1 in Growing Rats.

Author: Ruchi TRIPATHI ¹ ; Sanjay Kumar BANERJEE ^{2
,

3} ; Jay Prakash NIRALA ⁴ ; Rajani MATHUR ¹
Author Information

1. Department of Pharmacology, Delhi Institute of Pharmaceutical Sciences & Research, Delhi Pharmaceutical Sciences and Research University (DPSR-U), New Delhi, INDIA.
2. Drug Discovery Research Centre, Translational Health Science and Technology Institute, Faridabad, INDIA
3. Department of Biotechnology, National Institute of Pharmaceutical Education and Research, Guwahati, INDIA.
4. School of Environmental Sciences, Jawaharlal Nehru University, New Delhi, INDIA.
Publication Type:Journal Article
Keywords: Antioxidant system; Childhood-adolescence; EMF-mobile phone; Fructose; Hepatic insulin resistance; Hypothalamic insulin resistance; Insulin receptor signal; Mitochondrial OXPHOS
MeSH: Humans; Rats; Animals; Adult; Rats, Wistar; Fructose/metabolism*; Catalase; Receptor, Insulin/metabolism*; AMP-Activated Protein Kinases/metabolism*; Electromagnetic Fields/adverse effects*; Sirtuin 1/metabolism*; Cell Phone; Phosphatidylinositol 3-Kinases/metabolism*; Forkhead Box Protein O1/metabolism*; Uncoupling Protein 2
From: Biomedical and Environmental Sciences 2023;36(11):1045-1058
CountryChina
Language:English
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 < 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 < 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.