Introduction:
The obesogen hypothesis suggests that certain chemicals and pollutants act as obesogens. These obesogens promote obesity by altering the body's fat-storage metabolism. These chemicals may be present in various sources, such as pesticides, personal care products, and plastics. These obesogens may disturb the endocrine system, resulting in weight gain and other metabolic disorders that cause health problems. Obesogens act by altering the function of the hormones and other signaling molecules in the body, leading to fat cell development, appetite control, and a change in metabolism. However, the obesogen hypothesis suggests a potential for growing rates of obesity in recent years. More research has to be done to understand the effects of obesogens on human health.
What Are Obesogens?
Obesogens are chemicals that promote weight gain and obesity by altering the metabolism and fat storage in the body. In addition, they disrupt the normal regulation of the energy balance in the body by interfering with the hormones and other signaling molecules.
What Are the Chemical Obesogens?
Chemical obesogens can alter how the body stores and processes fat, affecting the hormones that regulate metabolism and appetite.
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Bisphenol A: BPA exposure during development increases body weight and adiposity across the lifespan. The effects of BPA were mediated through estrogen receptors. Several studies have failed to find a direct association between BPA and weight gain, suggesting the need for more research to delineate the effects of BPA on the metabolic systems, including the importance of diet, animal species, and doses, strain, and timing of exposures in the BPA effect on weight gain. Early life exposure leads to sexually dimorphic alterations in the structure of hypothalamic energy balance leading to increased vulnerability to glucose intolerance.
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Flame Retardants: Flame retardants are chemicals applied to various materials, including electronics, furniture, and construction materials, to reduce flammability or delay combustion. Polybrominated biphenyls and polybrominated diphenyl ethers were widely used as flame retardants. PBDEs have been detected at active levels in most people with various adverse health outcomes, including reduced thyroid function and obesity. In addition, prenatal and neonatal exposure is associated with low birth weight and thyroid function in the offspring. Effects noted include:
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Advanced female puberty that continues to adulthood.
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Male cardiac hypertrophy.
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Increased serum thyroxine levels.
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Reduced hepatic carboxylesterase activity in the dams.
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Air Pollution: Polycyclic aromatic hydrocarbons are the family of environmental chemicals that occur in coal, oil, and tar deposits and are produced as fuel burning, including cigarette smoke, and burning fuel, including diesel exhaust. Benzopyrene is a compound that has been shown to inhibit lipolysis and cause increased fat in adult mice. A recent study shows that pregnant women using personal air monitors during the second trimester had higher prenatal exposures associated with increased body size of children aged five and seven. Animals exposed to diesel exhaust during the development and high-fat diet as adults showed increased susceptibility to diet-induced weight gain and neuroinflammation later in life. In mice, early life exposure to air pollution particulates leads to increased visceral obesity, inflammation, and insulin resistance. Components of air pollution are most needed in animal models and humans to establish a causal relationship.
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High Fructose Corn Syrup: Sugars have been increasingly linked with obesity when consuming large amounts of sweetened soda. Growing evidence shows that obesogenic effects in dietary sugars were mainly due to the fructose content. Sucrose is 50 percent glucose and 50 percent fructose. These are fructose components and the most problematic. In addition, fructose was commercially derived from sugar cane, maize, and sugar beets, processed mainly into high fructose corn syrup. Fructose is commonly added to foods and drinks for palatability, and taste enhancement for baked goods. The glycemic index of fructose was lower than that of glucose. The majority of fructose quickly metabolizes in the liver without inducing insulin secretion. This is why the low doses of fructose help regulate glucose homeostasis at higher doses that are ingested. Excess fat is secreted in the form of low-density lipoprotein associated with type 2 diabetes. Fructose results in lipogenesis in the liver and thus obesogen by stimulating fat storage in the liver, as opposed to the adipocyte. Increasing the palatability of food by adding sucrose undermines the normal signals and motivates the energy intake independent of the needed energy. Obesogens developmental exposures to fructose can increase the susceptibility to obesity later in life.
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Transgenerational Obesogenic Transmission: The low dose of exposure to EDCs typically does not damage DNA rather than causing damage to the epigenetic profile for creating permanent change in the germline. For example, exposure to certain pesticides, fungicides, plastics, and air pollution that are linked to ovarian diseases. Maternal exposure to BPA has been linked to social and behavioral changes in epigenetic changes in the imprinted genes. Prenatal exposure of pregnant mice to TBT led to increased heavy depot weight, larger adipocyte size, and biased cell fate in the mesenchymal stem cell compartment to favor the adipocyte formation. Prenatal tributyl exposure led to fatty liver in all three generations. Effects of life in early exposure to at least some of the obesogens are transgenerational and permanent, increasing the risk of future generations for developing obesity and related disorders.
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Obesogen Screens: The obesogen hypothesis is critical to developing reproducible, robust, and sensitive assays to screen large numbers of chemicals for obesogenic properties. Several screens have been developed to meet these criteria in the past few years.
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In Vitro Assays: In vitro cell models allow for fast and systemic signaling pathways targeting. That is linked to obesity in humans. For example, it is a strongly expressed common obesogen target in the adipose tissue, essential for the differentiation of fatty tissue.
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In Vivo Assays: Animal assays with the fish and the other organisms allow the examination of multiple points for multiple hormones and mechanisms of action. Zebrafish was a good model in that metabolism can possess all the key organs required for metabolism control in humans, from the appetite circuits present in the hypothalamus through the pancreas and the insulin-sensitive tissues such as (the liver, white adipose tissue, and muscle).
Conclusion:
Metabolism is based on a complex process that involves many hormones. Such as insulin, glucocorticoids, androgens, estrogens, and thyroid hormones. These hormones control adipose tissue development, metabolism, and body weight.
