In an article published on March 22, 2016 in the peer-reviewed journal Endocrinology, Jonathan Boucher and colleagues from the Environmental Health Science and Research Bureau of Health Canada, Ottawa, Canada, report on the adipogenic effects of bisphenol S (BPS, CAS 80-09-1) in primary human preadipocytes obtained from female donors. BPS is often used as an alternative to bisphenol A (BPA, CAS 80-05-7) in food contact plastics and coatings. In their 2014 study, the same group had demonstrated adipogenic effects of BPA in a similar system. Further, in their 2015 study, Boucher and colleagues showed that glucuronidated metabolite of BPA, BPA-G, is also adipogenic (FPF reported).

Lipid accumulation in preadipocytes was increased about 4 times upon exposure to 25µM (approx. 6.3 mg/L) of BPS. Exposure to lower concentrations (0.1 nM – 10 µM) resulted in 1.5-2 fold increases, not being statistically significant. The mRNA expression of peroxisome proliferator-activated receptor γ (PPARγ), a key transcription factor involved in adipogenesis, increased in response to both low (0.1 nM) and high (25 µM) BPS concentrations (other concentrations were not tested). The mRNA levels of other adipogenic genes (CCAAT-enhancer-binding protein-α (CEBPα) and sterol regulatory element binding transcription factor 1 (SREBF1)), as well as markers of mature adipocytes (lipoprotein lipase (LPL), adipocyte protein 2 (aP2) and perilipin (PLIN)), could be increased only by high BPS concentration. On the protein level, the expression of aP2 and LPL (the only two proteins assessed) was induced by 10 and 25 µM, but not by lower BPS concentrations. In an in vitro reporter gene assay, the transcriptional activity of PPARγ promoter could be induced by 25 µM BPS. On the human aP2 promoter, glucocorticoid receptor (another transcription factor commonly associated with obesity) was shown to be a coactivator necessary for the induction of aP2 through interaction of BPS with PPARγ.

According to the authors, this study is a first report on the ability of BPS to induce lipid accumulation and differentiation in primary human preadipocytes, likely through direct activation of PPARγ. Noteworthy, statistically significant BPS effects on lipid accumulation were observed at rather high concentrations, not likely to occur physiologically. However, PPARγ expression was affected at much lower BPS concentrations. Overall, further research is necessary to confirm the role of BPS in the etiology of obesity. However, already now it is clear that many actions of BPS may be similar to those of BPA, as has been discussed repeatedly (FPF reported).


Boucher, J. et al. (2016). “Bisphenol S induces adipogenesis in primary human preadipocytes from female donors.Endocrinology 157:1397-1407.

Boucher, J. et al. (2015). “In vitro effects of bisphenol A β-D-glucuronide (BPA-G) on adipogenesis in human and murine preadipocytes.Environmental Health Perspectives 123:1287-1293.

Boucher, J. et al. (2014). “Bisphenol A induces differentiation of human preadipocytes in the absence of glucocorticoid and is inhibited by an estrogen-receptor antagonist.”  Nutrition & Diabetes 4:e102.