Triclosan (TCS) promotes lipid accumulation in the mouse adipocyte (3T3-L1) cell line via peroxisome proliferator activated receptor gamma (PPARγ) pathway

Abstract

Triclosan (TCS) is one of the most widely used antibacterial agents and is commonly detected not only in the environment but also in the human body. Epidemiological studies have associated TCS exposure with increased body weight and metabolic alterations. The aim of this study was to elucidate the molecular mechanisms by which TCS promotes lipid accumulation and differentiation in preadipocytes, using the murine 3T3-L1 cell model. Our experiments demonstrate that low concentrations of TCS (1 μM) promote lipid accumulation and induce adipogenic differentiation in 3T3-L1 cells. This process involves PPARγ-related pathways, as confirmed using rosiglitazone, a well-characterized PPARγ agonist. TCS further potentiates rosiglitazone-induced differentiation, leading to the formation of mature adipocytes with large lipid droplets. This phenotype is associated with reduced levels of GLUT4 and IGF-1R, i.e. key regulators of glucose uptake and insulin signaling. Additionally, TCS modulated the expression of adipogenic and metabolic regulators, including FABP4, Resistin, DLK1, Adipoq, Serpin E1, and VEGF-A. TCS also altered the activity of signaling proteins such as PI3K, STAT3, and GSK3β. Notably, at the tested concentration, TCS did not affect the IκBα/NFκB axis, suggesting it does not trigger inflammatory signaling in this model. Our findings indicate that TCS enhances 3T3-L1 differentiation toward a metabolically compromised adipocyte phenotype, supporting its classification as a potential pro-obesogenic compound. These results provide new insights into how TCS may contribute to adipose tissue dysfunction and the development of insulin resistance. Further in vivo studies are warranted to assess the systemic impact of chronic TCS exposure.