Bisphenols are a group of industrial chemicals widely used in the manufacture of plastics and epoxy resins. Bisphenol F (BPF) is increasingly being used as a substitute for bisphenol A (BPA), which is a widely used environmental endocrine-disrupting chemical (EDC) and hypothesized obesogen. Nevertheless, limited research has examined the potential of BPF to induce obesity, leaving a knowledge gap. To address this issue, this study investigated the effect of BPF on the differentiation of 3T3-L1 preadipocyte and its underlying mechanisms. 3T3-L1 preadipocytes were cultured and induced to differentiate in controlled conditions, then exposed to varying BPF doses over an 8-day period. Significant increases in intracellular lipid droplets and triglyceride (TG) content were observed in the treated cells, indicating that BPF has a stimulating effect on adipogenesis. In BPF-treated 3T3-L1 preadipocytes, key adipogenic genes and proteins, including peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein alpha (C/EBPα), adiponectin and fatty acid-binding protein 4 (FABP4) in 3T3-L1 preadipocytes was significantly upregulated. Further treatment with estrogen receptor (ER) antagonist ICI 182780 and PI3K inhibitor LY 294002 revealed that BPF could promote differentiation of 3T3-L1 preadipocytes through the ER mediated phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. In summary, BPF may enhance the maturation of 3T3-L1 preadipocytes by activating the ER-PI3K/AKT pathway, potentially contributing to obesity. These findings enhance the understanding of the obesogenic properties of environmental chemicals and could inform new strategies for preventing and managing obesity.
Background: Depression may be influenced by environmental factors, including phthalate exposure as endocrine-disrupting chemicals (EDCs). Gut microbiota may modulate phthalate toxicity, and probiotics have been shown to alleviate depressive symptoms; however, their interrelationship remains unclear.
Methods: This cross-sectional study included 7999 participants from the 2005-2018 National Health and Nutrition Examination Survey (NHANES). Data on probiotic/yogurt consumption, urinary phthalate metabolites, depressive symptoms (measured by PHQ-9), and covariates were collected. Weighted generalized linear models (W-GLM) were employed to elucidate variable associations. Mediation analyses assessed whether phthalates mediated the association between probiotic/yogurt consumption and depressive symptoms. Similarly, subgroup analyses were conducted to elucidate sex-specific differences.
Results: The data revealed that probiotic/yogurt consumption was significantly associated with lower PHQ-9 scores. Furthermore, probiotic/yogurt consumption was inversely associated with urinary MBzP and MiBP levels, with MiBP mediating 7 % of its association with depressive symptoms. Multiple-group mediation analysis showed that the mediating effect was significant in females only, indicating possible sex-specific mechanisms.
Conclusions: Probiotic/yogurt consumption may be linked to reduced depressive symptoms via lowered phthalate exposure, particularly MiBP. Phthalates affect females more than males, suggesting sex-specific susceptibility to EDCs. Further studies are required to validate the underlying molecular mechanisms.

