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Updated: Jan 7, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Endocrine disruptors, obesity, and metabolic syndrome
Tuğba Barlas1, Alev Eroğlu Altinova1, Meriç Coşkun1
1Division of Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, Gazi University, Ankara, Turkiye.
Abstract:
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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