PFOS Triggers Atypical Fat Cell Growth and Metabolic Shifts — A Newly Uncovered Health Concern

To discover the impact of exposure to PFOS, a type of endocrine‑disrupting chemical that can be found easily in daily life, Professor Chris WONG and Dr Jamie WAN from the Department of Biology led a research team and conducted a series of studies.

In a recent study, the team explored how PFOS influences fat cell development and lipid metabolism in mouse 3T3-L1 preadipocytes. PFOS promoted the formation of fat cells, leading to increased oil droplets within cells and higher levels of markers such as PPARγ, perilipin, FABP4, LPL, CD36, FASN, and GLUT4. It also boosted hormones related to fat, such as adiponectin and resistin. Compared with troglitazone (TGZ), a well-known PPARγ activator, PFOS had milder effects on fat cell development. When combined, PFOS lessened TGZ's ability to promote fat cell formation, indicating they might interfere with each other. PFOS also influenced a type of RNA modification, m6A, by altering enzyme activity, suggesting that it regulates fat-related genes post-transcriptionally. Functional tests showed that PFOS maintained forskolin-stimulated fat breakdown (lipolysis) at normal levels, without slowing it. Interestingly, it increased metabolic markers, such as CPT1a, PDHK, and FGF21, and raised ATP levels in the PFOS group. These molecular changes hint at increased energy use or stress, even though the cells still resembled white fat cells.

Overall, these various effects probably stem from PFOS's impact on PPARγ signaling and m6A RNA modifications. By examining these mechanisms, the study helps us better understand potential metabolic risks associated with PFOS exposure.

The research findings have been published in Environmental Science and Technology Letters under the title “Perfluorooctane Sulfonate Induces an Atypical Adipocyte Phenotype: Promoting Adipogenesis and Thermogenesis via PPARγ Signaling and m6A RNA Modifications in 3T3-L1 Cells”.

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