Author(s):
Seewooruttun C*, Bouguila B, Corona A, Delanaud S, Bodin R, Bach V, Desailloud R, Pelletier A.
* PériTox (UMR I_01), UPJV/INERIS, University of Picardy Jules Verne, CURS, Chemin du Thil, 80025 Amiens.
France
Published in:
Int J Mol Sci 2025; 26 (6): 2792
Published: 20.03.2025
on EMF:data since 05.05.2025
Further publications: Study funded by:

The French National Research Program for Environmental and Occupational Health of Anses (ANSES-21-RF-10).

Keywords for this study:
Gene/protein expression (general)
Medical/biological studies
Go to EMF:data assessment

5G Radiofrequency Exposure Reduces PRDM16 and C/EBP β mRNA Expression, Two Key Biomarkers for Brown Adipogenesis.

Original Abstract

The widespread use of wireless technologies has raised public health concerns about the biological effects of radiofrequency (RF) exposure. Children have a higher specific absorption rate (SAR) of radiation energy compared to adults. Furthermore, brown adipose tissue (BAT) is more prevalent in infants and tends to decrease with age. Previous animal studies demonstrated a cold sensation in rats exposed to 900 MHz (second generation, 2G). UCP1-dependent thermogenesis and BAT hyperplasia are two fundamental adaptive mechanisms initiated in response to cold. This study investigated the impact of short-term exposure to 2G and fifth generation (5G) on key thermogenic and adipogenic markers related to these mechanisms while considering age and exposure duration. Juvenile and young adult Wistar rats were randomized into three subgroups: a 5G group (3.5 GHz), 2G group (900 MHz), and a control group (SHAM). They were exposed to their respective continuous-wave RF signals for 1 or 2 weeks at an intensity of 1.5 V/m, with two exposure sessions of 1 h per day. After the exposure period, a RT-qPCR was carried out to evaluate the genetic markers involved in BAT thermogenesis and adipogenesis. Two adipogenic biomarkers were affected; a fold change reduction of 49% and 32% was detected for PRDM16 (p = 0.016) and C/EBP β (p = 0.0002), respectively, after 5G exposure, regardless of age and exposure duration. No significant RF effect was found on UCP1-dependent thermogenesis at a transcriptional level. These findings suggest that exposure to a 5G radiofrequency may partially disrupt brown adipocyte differentiation and thermogenic function by downregulating PRDM16 and C/EBP β, possibly leading to higher cold sensitivity.

Keywords

radiofrequency | brown adipose tissue | UCP1-dependent thermogenesis | brown adipogenesis | rat model

Exposure:

900 MHz
3500 MHz
5G
Ganzkörper-SAR = 0,07 mW/kg (3500 MHz / 5G); 0,24 mW/kg (900 MHz / 2G)

EMF:data assessment

Summary

Although 5G technology offers remarkable speed improvements, concerns about its long-term health effects remain. Brown adipose tissue (BAT) is essential for generating heat in mammals, particularly in children, where it is most prevalent. It naturally declines with age. Moreover, children absorb a higher proportion of radiofrequency energy than adults, making them more susceptible to the potential effects of radiofrequency electromagnetic fields (RF-EMF). Previous animal studies have shown that low-intensity RF-EMF can stimulate cold-defense responses, such as vasoconstriction and altered norepinephrine levels. Two primary mechanisms underpin cold-induced brown adipose tissue (BAT) activation: UCP1-dependent thermogenesis and brown adipocyte hyperplasia. This study explores how 2G and 5G exposure impacts genes central to BAT thermogenesis and adipogenesis in juvenile versus young adult rats. The aim is to clarify the age- and duration-dependent impacts and potential metabolic risks.

Source: ElektrosmogReport | Issue 2/2025

Study design and methods

Sixty male Wistar rats, aged either 3 weeks (juvenile) or 8 weeks (young adult), were divided into three groups: a sham-exposed control group and two exposure groups (2G at 900 MHz and 5G at 3.5 GHz). Each group (n = 5) underwent either one or two weeks of exposure. The animals were exposed twice daily for one hour at 1.5 V/m, corresponding to whole-body SAR values of 0.07 mW/kg (5G) and 0.24 mW/kg (2G). After exposure, the interscapular BAT was collected and analyzed by quantitative PCR to determine the mRNA levels of thermogenic markers (UCP1, UCP3, PGC1α, PPARα, PPARγ, Cidea, ADRß3, S100b) and adipogenic markers (PRDM16, C/EBP β, C/EBP α, Zfp423).

Results

5G exposure induced a significant downregulation of adipogenic transcription factors PRDM16 (-49%), C/EBP β (-32%), and Zfp423 (-30%), regardless of age and exposure duration. In contrast, 2G exposure produced an age-dependent decrease in PPARα only in young adult rats. ADRß3 expression increased under both 2G and 5G conditions in a duration-dependent manner: juvenile rats exhibited a significant increase only after one week of exposure.

Conclusions

The authors conclude that 5G radiofrequency exposure may impair brown adipocyte differentiation by downregulating PRDM16, C/EBP β, and Zfp423, thereby reducing BAT-mediated heat production and increasing cold sensitivity. The core UCP1 thermogenic pathway appears unaffected by RF-EMF. Alterations in PPARα and ADRβ3 suggest exposure- and age-specific effects of RF-EMF on brown fat biology.

Editor's note:

The extremely low field strengths and SAR values at which non-thermal effects occur are alarming. ICNIRP limits for the general public allow up to 0.08 W/kg, which is roughly a thousand times higher than the 0.07 mW/kg used for 5G in this study. The lack of frequency modulation in the experimental fields suggests that real-world 5G signals could have an even greater biological impact (Lai & Levitt, 2022). Study limitations include small group sizes (n = 5) and the absence of proteomic validation –mRNA changes may not translate to altered protein levels. Intriguingly, low-intensity radiofrequency electromagnetic fields (RF-EMF) may indeed disrupt mammalian thermoregulation. (RH)

Lai H, Levitt BB. (2022). The roles of intensity, exposure duration, and modulation on the biological effects of radiofrequency radiation and exposure guidelines. In Electromagnetic Biology and Medicine (Vol. 41, Issue 2, pp. 230–255). Taylor & Francis. https://doi.org/10.1080/15368378.2022.2065683