ENDOCRINE DISRUPTORS AND ENVIRONMENTAL OBESOGENS: MECHANISM LINKING CHEMICAL EXPOSURE TO OBESITY AND METABOLIC COMORBIDITIES

Obesity is a growing global public health challenge traditionally attributed to excessive energy intake, physical inactivity, genetic predisposition, and socioeconomic factors. However, emerging evidence suggests that environmental exposures may also influence metabolic regulation and susceptibility to obesity. This review examines endocrine-disrupting chemicals (EDCs) and environmental obesogens, focusing on their sources, molecular mechanisms, metabolic consequences, and implications for public health. Major chemical classes, including bisphenols, phthalates, per- and polyfluoroalkyl substances (PFAS), selected pesticides, and organotins, are discussed in relation to their potential effects on adipogenesis, nuclear receptor signalling, lipid accumulation, and epigenetic regulation. The review further explores associations between obesogen exposure and metabolic comorbidities, including insulin resistance, type 2 diabetes mellitus, dyslipidaemia, metabolic dysfunction-associated steatotic liver disease, cardiovascular risk, and reproductive dysfunction. Evidence from experimental models and human epidemiological studies is critically evaluated, emphasizing limitations in causal inference, exposure assessment, dose–response relationships, and chemical mixture analysis. Biomonitoring, regulatory frameworks, safer chemical substitution, and emerging research approaches are also considered. Although experimental findings support the biological plausibility of obesogenic effects, human evidence remains heterogeneous across chemical classes and populations. Integrating mechanistic research, longitudinal epidemiology, and environmental risk assessment is essential to clarify causal relationships and inform effective strategies for reducing chemical exposure and preventing obesity-related metabolic complications.