Understanding the myriad of factors contributing to obesity is essential for
curbing its decade-long expansion. Recently, despite the evidence of traditional
contributing factors, the role of environmental chemicals with endocrine disrupting
activity has also been highlighted. Undeniably, even very small concentrations of these
endocrine disrupting chemicals (EDCs) have the capacity to induce severe health
damages. The “environmental obesogen” hypothesis associates EDCs to the disruption
of energy homeostasis, in particular because of their ability to modulate adipocyte
biology. Further studies have revealed numerous potential mechanisms, including
modulation of nuclear hormone receptor function and modification of the epigenome.
More recently, their involvement in exacerbating metabolic dysfunction in an obesity
context reinforces the hypothesis that EDCs have an important “environmental
dysmetabolic” effect. Besides adulthood exposure, the perinatal effects are very
important since they may allow a change in metabolic programming, encouraging the
further development of obesity. Consequently, additional research directed at
understanding the nature and action of EDCs will illuminate the connection between
health and environment as well as the possible effects triggered by these compounds in
respect to public health. Nutrition is being further substantiated as an important
modulator of inflammatory and antioxidant pathways, especially associated with
environmental insult; nutrition is also emerging as a tool to address exposure toxicity of
ECDs as both a sensing and remediation platform. Ultimately, improving EDC
exposure measurement, reducing confounding bias, identifying discrete periods of
vulnerability and quantifying the effects of EDC mixtures will enhance inferences
originated from epidemiological studies.
Keywords: Adipose tissue, Adipocytes, Cardiometabolic disease, Endocrine
disrupting chemicals, Epigenetics, Inflammation, Metabolic syndrome,
Metabolism-disrupting chemicals, Microbiota, Nutrition, Obesity, Obesity
paradox, Obesogens, Type 2 diabetes.
