leptin and bis(4-hydroxyphenyl)sulfone

Bisphenol A (BPA) has been widely reported to exert endocrine disrupting effects, including the induction of adipogenesis in cultured preadipocytes and intact animals. Because of the potential harm to human health, BPA is being substituted by structurally related bisphenols. Whether or not such BPA analogues are safe substitutes, however, remains largely unknown. Here, we investigated the potential of bisphenol B (BPB), bisphenol E (BPE), bisphenol F (BPF), bisphenol S (BPS), and 4-cumylphenol (4-CP) to affect lipid and hormone levels in 3 T3-L1 cells. We found that BPB, BPE, BPF, BPS, and 4-CP all affected lipid accumulation and leptin levels to the same extent and potencies as BPA. Based on these and other results, we conclude that these BPA analogues and 4-CP most likely will elicit similar effects on adipocytes as BPA. Using them to substitute BPA in products should be done with caution.

Topics: 3T3-L1 Cells; Adipocytes; Animals; Benzhydryl Compounds; Biomarkers; Cell Survival; Endocrine Disruptors; Humans; Leptin; Lipid Metabolism; Mice; Phenols; Sulfones; Transcriptome

As bisphenol A (BPA) has been shown to induce adverse effects on human health, especially through the activation of endocrine pathways, it is about to be withdrawn from the European market and replaced by analogues such as bisphenol S (BPS). However, toxicological data on BPS is scarce, and so it is necessary to evaluate the possible effects of this compound on human health. We compared the effect of BPA and BPS on obesity and hepatic steatosis processes using low doses in the same range as those found in the environment. Two in vitro models were used, the adipose cell line 3T3-L1 and HepG2 cells, representative of hepatic functions. We analyzed different parameters such as lipid and glucose uptakes, lipolysis, leptin production and the modulation of genes involved in lipid metabolism and energy balance. BPA and BPS induced an increase in the lipid content in the 3T3-L1 cell line and more moderately in the hepatic cells. We also observed a decrease in lipolysis after bisphenol treatment of adipocytes, but only BPS was involved in the increase in glucose uptake and leptin production. These latter effects could be linked to the modulation of SREBP-1c, PPARγ, aP2 and ERRα and γ genes after exposure to BPA, whereas BPS seems to target the PGC1α and the ERRγ genes. The findings suggest that both BPA and BPS could be involved in obesity and steatosis processes, but through two different metabolic pathways.

Topics: 3T3-L1 Cells; Adipocytes; Animals; Benzhydryl Compounds; Glucose; Hep G2 Cells; Humans; Leptin; Lipolysis; Liver; Mice; Phenols; PPAR gamma; Receptors, Estrogen; Sulfones; Triglycerides