Amongst the many environmental factors that can promote the development of excess weight gain, one of the most intriguing and persistent notions is the possible role of obesogenic environmental toxins.
No doubt, the presence of environmental pollutants is associated with “westernisation” and many organic pollutants tend to accumulate in adipose tissue where they can have substantial metabolic effects – at least in theory.
But how good is the evidence that environmental pollutants can in fact affect adipocyte growth and function?
This issue was recently addressed by Robert Sargis and colleagues from the University of Chicago, IL, in a study just published in OBESITY.
This study focused on the potential contributions of environmental pollutants that act as endocrine disrupting chemicals (EDCs) on glucocorticoid signaling, a major driver of adipogenesis.
The researchers screened various EDCs and found that bisphenol A (BPA), dicyclohexyl phthalate (DCHP), endrin, and tolylfluanid (TF)) had significant stimulatory effects on the glucocorticoid receptor. Amazingly, even minute (picomolar) quantities of these compounds markedly promoted lipid accumulation and adipocyte differentiation in 3T3-L1 preadipocytes.
Importantly, these effects required the presence of a weak differentiating cocktail suggesting that the effects of these compounds is mediated through synergistic effects with known modulators of adipocyte differentiation. Thus, these compounds appear to act as “accelerators” rather than “inducers” of fat formation.
These findings raise a number of interesting possibilities: for e.g. I cannot help but wonder whether drinking sugary pop out of a glass bottle is perhaps less obesogenic than drinking the same number of calories out of a BPA containing plastic bottle or can?