Depot-specific analysis of human adipose cells and their responses to Bisphenol S

Exposure to endocrine disrupting chemicals (EDCs) is associated with adverse health outcomes including obesity and diabetes.  Obesity, and more specifically visceral obesity, is correlated with metabolic disease.  The adipose tissue is an endocrine organ and a potential target for many environmental pollutants including bisphenols.  The subcutaneous and the omental (visceral) depots are comprised of mature adipocytes and residing progenitors, which may be different between the depots and may be EDCs targets.  Bisphenol A (BPA) is a suspected metabolic disruptor, and is being replaced with structurally similar compounds such as bisphenol S (BPS).  Like BPA, BPS induces adipogenesis in murine and primary human subcutaneous preadipocytes.  However, the effect of BPS on omental preadipocytes is not known.  In this study, we show that human primary progenitors from omental depots have a distinct transcriptomic signature as compared to progenitors derived from donor-matched subcutaneous depots.  Furthermore, we show that BPS increases adipogenesis of both omental and subcutaneous preadipocytes and can mimic the action of glucocorticoids or peroxisome proliferator-activated receptor g (PPARg) agonists.  We also show that BPS treatment, at 0.1 µM and 25 µM, modifies the adipokine profiles of both omental and subcutaneous derived adipocytes, in a depot specific manner.  Taken together our data show distinct gene expression profiles in the omental versus subcutaneous progenitors and similar responses to the BPA analogue, BPS.