Abstract
Adult and childhood obesity have reached pandemic level proportions. The idea that caloric excess and insufficient levels of physical activity leads to obesity is a commonly accepted answer for unwanted weight gain. This paradigm offers an inconclusive explanation as the world continually moves towards an unhealthier and heavier existence irrespective of energy balance. Endocrine disrupting chemicals (EDCs) are chemicals that resemble natural hormones and disrupt endocrine function by interfering with the body’s endogenous hormones. A subset of EDCs called obesogens have been found to cause metabolic disruptions such as increased fat storage, in vivo. Obesogens act on the metabolic system through multiple avenues and have been found to affect the homeostasis of a variety of systems such as the gut microbiome and adipose tissue functioning. Obesogenic compounds have been shown to cause metabolic disturbances later in life that can even pass into multiple future generations, post exposure. The rising rates of obesity and related metabolic disease are demanding increasing attention on chemical screening efforts and worldwide preventative strategies to keep the public and future generations safe. This review addresses the most current findings on known obesogens and their effects on the metabolic system, the mechanisms of action through which they act upon, and the screening efforts through which they were identified with. The interplay between obesogens, brown adipose tissue, and the gut microbiome are major topics that will be covered.
Highlights
Specialty section: This article was submitted to Translational Endocrinology, a section of the journal Frontiers in Endocrinology
More recent studies testing the safety of Bisphenol S (BPS), a Bisphenol A (BPA) substitute used in the manufacturing of plastics, have used in vivo mouse models to determine if BPS exhibits obesogenic properties by affecting gene expression and DNA methylation
This may lead to high levels of inflammation, which is known to lead to dysregulation of insulin signaling, GLP1 secretion from the intestine [190], and interfere with adipogenesis through the aryl hydrocarbon receptor (AhR) [230]
Summary
Obesity has become a present-day pandemic affecting people of all ages across the world. The prevalence of obesity in children has continued to rise in the U.S alone, despite the nation’s efforts to promote better nutrition practices and increase physical activity levels in the educational system [2]. Obesity often presents together with depression and negative self-image in both children and adults, creating a vicious cycle where the conditions potentiate each other [3, 6]. Many types of fad diets have shown short-lived improvements in body weight, but the overall success for long-term weight loss through caloric restriction remains inefficacious and the global prevalence of obesity continues to rise. Some lower income countries have reported a decrease in exercise, other higher income countries, such as the U.S, have reported a consistent or even increased level of exercise over the last 30 years despite the continuous rise in obesity [12, 13]. The current caloric models of obesity and weight gain are insufficient as stand-alone explanations for the sudden increase in global obesity over the past few decades
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