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Endocrine disruptors, obesity, and metabolic syndrome

Journal of Invertebrate Pathology 2025 2 citations

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Endocrine-disrupting chemicals found in plastics—including bisphenols, phthalates, and PFAS—act as obesogens by interfering with adipogenesis pathways, gut microbiota, and hormonal appetite regulation, contributing to the global rise in obesity and metabolic syndrome. This review reinforces that plastic-associated chemical exposures carry systemic metabolic health risks beyond physical microplastic particle ingestion.

The global prevalence of obesity and metabolic syndrome (MetS) is rising worldwide, and increasing evidence suggests that chemical exposures-particularly endocrine disruptors (EDs)-represent a significant contributing factor. EDs can act as obesogens, increasing the risk of weight gain and related metabolic conditions, including type 2 diabetes, dyslipidemia, hypertension, and cardiovascular disease. They may also alter the basal metabolic rate, gut microbiota composition, and hormonal regulation of appetite and satiety. EDs are reported to exert their effects mainly through the peroxisome proliferator-activated receptor gamma pathway, which is primarily expressed in adipose tissue and is a key regulator of adipogenesis. Common consumer products such as plastic bottles, metal food cans, detergents, toys, cosmetics, and pesticides frequently contain EDs. Humans can be exposed to these chemicals via multiple routes, including transplacental transfer, breast milk, inhalation, ingestion, and dermal absorption. Bisphenols, tributyltin, phthalates, per- and polyfluoroalkyl substances, polycyclic aromatic hydrocarbons, and heavy metals are among the known EDs that have been associated with obesity and MetS. The need for further investigation and stricter regulations to mitigate the public health consequences of environmental exposure to EDs is consistently emphasized in recent literature. Understanding the mechanisms by which EDs affect various hormones and systems is essential for developing effective prevention and intervention strategies. In this review, we discuss the relationship between obesity, MetS, and EDs, along with exposure pathways and preventive strategies.

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