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    Obesogens and Energy Homeostasis: Definition, Mechanisms of Action, Exposure, and Adverse Effects on Human Health
    (Karger, 2025) Yilmaz, Bayram; Erdogan, Cihan Suleyman; Sandal, Suleyman; Kelestimur, Fahrettin; Carpenter, David O.
    Background: Obesity is a major risk factor for non- communicable diseases and is associated with a reduced life expectancy of up to 20 years, as well as with other consequences such as unemployment and increased economic burden for society. It is a multifactorial disease, and physiopathology of obesity involves dysregulated calorie utilization and energy balance, disrupted homeostasis of appetite and satiety, lifestyle factors including sedentary lifestyle, lower socioeconomic status, genetic predisposition, epigenetics, and environmental factors. Some endocrine- disrupting chemicals (EDCs) have been proposed as obesogens that stimulate adipogenesis leading to obesity. In this review, definition of obesogens, their adverse effects, underlying mechanisms, and metabolic implications will be updated and discussed. Summary: Disruption of lipid homeostasis by EDCs involves multiple mechanisms including increase in the number and size of adipocytes, disruption of endocrine-regulated adiposity and metabolism, alteration of hypothalamic regulation of appetite, satiety, food preference and energy balance, and modification of insulin sensitivity in the liver, skeletal muscle, pancreas, gastrointestinal system, and the brain. At a cellular level, obesogens can exert their endocrine disruptive effects by interfering with peroxisome proliferator-activated receptors and steroid receptors. Human exposure to chemical obesogens mainly occurs by ingestion and, to some extent, by inhalation and dermal uptake, usually in an unconscious manner. Persistent pollutants are lipophilic features; thus, they bioaccumulate in adipose tissue. Key Messages: Although there are an increasing number of reports studying the effects of obesogens, their mechanisms of action remain to be elucidated. In addition, epidemiological studies are needed in order to evaluate human exposure to obesogens.
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    PCB 9 exposure induces endothelial cell death while increasing intracellular calcium and ROS levels
    (Wiley, 2012) Yilmaz, Bayram; Sandal, Suleyman; Carpenter, David O.
    Cultured porcine endothelial cells were used to determine the effects of several congeners of polychlorinated biphenyls (PCBs) on cell viability and changes induced by these congeners on levels of intracellular calcium and reactive oxygen species (ROS). Cultured endothelial cells were prepared as a single suspension and run on flow cytometry. Cell viability, intracellular calcium, and ROS concentrations were simultaneously determined by using propidium iodide, Fluo-3, and dihydrorodamine, respectively. The congeners tested included two coplanar tetrachlorinated congeners that have no ortho chlorines, PCBs 77 and 80, a tri-chloro congener which does not have any ortho chlorine, PCB 39, a di-ortho, tetrachlorinated congener, PCB 52, and a mono-ortho congener, PCB 9. PCB 9 was cytotoxic at 5 mu M within 5 min of exposure, and the toxicity increased with time and concentration. None of the other congeners showed consistent cytotoxicity. The cytotoxicity was roughly correlated with elevations in cellular ROS levels, but not with changes in intracellular calcium. To the best of our knowledge, toxicity of lower chlorinated, more volatile congeners such as PCB 9 has not been previously studied. These observations may be taken to explain the elevated risk of cardiovascular disease previously reported among residents living near to hazardous waste sites containing PCBs. (c) 2011 Wiley Periodicals, Inc. Environ Toxicol, 2012.