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.