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Human adipose tissue gene expression signatures indicate an inflammatory response and retinoic receptor activation under persistent organic pollutants exposure.
Environ. Adv. 21:100655 (2025)
Adipose tissue (AT) is subject to permanent accumulation of persistent organic pollutants (POP) due to their hydrophobic nature. Therefore, AT can be considered as interface between the body and an increasingly complex exposure to the chemical environment. As endocrinologically activate tissue, AT itself secretes adipokines regulating inflammation, insulin sensitivity and energy expenditure among others which are known to be dysfunctional in obesity. This study examined the impact of accumulated POPs 4,4-Diisoopropylbiphenyl (DIPB) and Ethyltetradecanoate (ETD) on human AT function. RNA-sequencing based gene expression analysis was conducted within the Leipzig Obesity Biobank (LOBB) between individuals (N = 43) with positive concentrations of DIPB and ETD in body fat against negative controls in subcutaneous (SAT) and visceral AT (VAT) in a sex-specific manner independent of their obesity status. Our study reveals sex- and AT-depot-specific gene expression profiles associated with immune responses, NF-κB signaling, and PPARγ pathways, highlighting POP interaction with immunological reactions in AT independent of obesity. Notably, our findings suggest altered retinoid acid receptor activity, which may influence AT browning. This research provides novel insights into the molecular mechanisms underlying the impact of POP exposure on human AT function. Importantly, our results indicate that POP exposure can contribute to AT dysfunction independently of obesity, suggesting that external environmental factors, such as POPs, should be considered as potential drivers of AT dysfunction in future obesity-related studies.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Adipose Tissue Dysfunction ; Gene Expression ; Obesity ; Persistent Organic Pollutants
ISSN (print) / ISBN
2666-7657
e-ISSN
2666-7657
Journal
Environmental Advances
Quellenangaben
Volume: 21,
Article Number: 100655
Publisher
Elsevier
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)