REVIEW article
Front. Endocrinol.
Sec. Translational and Clinical Endocrinology
Volume 16 - 2025 | doi: 10.3389/fendo.2025.1606654
Bisphenols Exposure and Non-Alcoholic Fatty Liver Disease: From Environmental Trigger to Molecular Pathogenesis
Provisionally accepted
- 1Department of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Qingdao University, Qingdao, China
- 2Department of Thoracic Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China
- 3Institute for Translational Medicine, Qingdao University, Qingdao, Shandong Province, China
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Bisphenols (BPs), including bisphenol A (BPA) and its substitutes (BPS, BPF), are ubiquitous environmental contaminants with emerging links to metabolic disorders. This review synthesizes current evidence on the role of BP exposure in the pathogenesis of nonalcoholic fatty liver disease (NAFLD), a global health crisis affecting 25% of adults worldwide. Epidemiological studies reveal significant positive associations between urinary/serum BP levels and NAFLD risk, particularly in males, with maternal exposure correlating to transgenerational metabolic dysfunction. Mechanistically, BPs disrupt hepatic lipid homeostasis by activating PPAR-γ and suppressing fatty acid oxidation while concurrently inducing insulin resistance via impaired IRS-1/PI3K/Akt signaling. Oxidative stress, NLRP3 inflammasome activation, and gut-liver axis perturbations further exacerbate steatosis and inflammation. Co-exposure with phthalates or high-fat diets amplifies hepatotoxicity, highlighting synergistic environmental risks. Critically, developmental and sexspecific susceptibility underscores the need for tailored interventions. We propose preventive strategies to mitigate NAFLD progression, including BP avoidance and policy reforms. This work bridges gaps between environmental epidemiology and molecular toxicology, emphasizing BPs as modifiable drivers of metabolic liver disease.
Keywords: Non-alcoholic fatty liver disease, Bisphenols, environmental epidemiology, molecular pathogenesis, bisphenol A
Received: 10 Apr 2025; Accepted: 29 Apr 2025.
Copyright: © 2025 Li, Yao, Zhang, Cui, Sun, Cao and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Jingyu Cao, Department of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Qingdao University, Qingdao, China
Zusen Wang, Department of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Qingdao University, Qingdao, China
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