A compound used to reduce public exposure to possible toxic effects of the chemical Bisphenol A (BPA) may cause impairment to fat cells, which could lead to widespread inflammation and obesity.
The first-of-its-kind study is published ahead of print in the American Journal of Physiology – Cell Physiology.
Recent studies suggest that, in addition to lifestyle causes, environmental factors may contribute to obesity in the U.S., including the exposure to endocrine-disrupting chemicals.
Endocrine-disrupting chemicals are substances that interrupt the function of the endocrine hormones that manage a variety of bodily processes, including metabolism and growth.
Previous research has found that BPA, used to make plastics such as water bottles, reusable food storage and the resins that line canned food containers, may leach into food and present a potential health hazard.
Some manufacturers that produce BPA-free products use a similar compound called Bisphenol AF (BPAF).
The possible endocrine-disrupting effects of BPAF have not been as widely studied as BPA in animals, and more importantly, people.
Researchers from Baylor College of Medicine in Houston studied preadipocytes – an immature form of fat cells – donated by healthy women to determine the effects of BPAF on inflammation and metabolic responses associated with obesity.
The research team treated the fat cells with BPAF and analyzed them as the cells matured. Exposure to BPAF increased lipid accumulation – the fat component in fat cells – and activated a protein that regulates the production of fat cells.
In addition, treatment with BPAF led to impairment of the cells’ energy centers (mitochondria) and increased expression of genes involved with inflammation. Inflammation in fat cells critically contributes to the complications of obesity and metabolic syndrome.
“It is difficult to determine, based on [lab-based] exposures, whether the potency of BPAF influences physiology sufficiently to affect the metabolic profile of obesity,” the researchers wrote.
“Nonetheless, the increased environmental accumulation of BPA alternatives motivates a need to understand how BPAF exerts effects on endocrine tissues,” they added.
“Bisphenol AF promotes inflammation in human white adipocytes” is published ahead of print in the American Journal of Physiology—Cell Physiology.
There is evidence that synthetic chemicals in our environment called, obesogens, may play an important role in the global obesity epidemic. Bisphenol A (BPA) is one of the most studied obesogens. Due to concerns surrounding the use of BPA, BPA structural analogues are being used as substitutes in consumer products.
However, there is currently little information available regarding their effects on pathways important for the development of obesity.
Interestingly, serotonin (5-HT) signaling in peripheral tissues plays an important role in regulating metabolic homeostasis.
Moreover, BPA has been shown to alter 5-HT signaling in the central nervous system.
Therefore, the objective of this study was to determine the effects of BPA analogues on adipogenesis and elucidate whether their obesogenic effects involve peripheral 5-HT signaling.
3T3-L1 preadipocytes were treated with 10 μM BPA or four commonly used BPA analogues during differentiation. Lipid accumulation was assessed by Oil Red O staining.
Adipogenic markers and genes important for 5-HT synthesis/metabolism were subsequently examined following treatment with BPA and the structural analogue bisphenol AF (BPAF).
The roles of tryptophan hydroxylase 1 (TPH1) and monoamine oxidase (MAO), in addition to glucocorticoid receptor (GR) signaling were also evaluated.
Treatment with 10 μM BPAF and Bisphenol S (BPS) significantly increased lipid accumulation in differentiated 3T3-L1 cells. 10 μM BPAF significantly increased adipogenic gene markers, as well as GR gene transcripts. Moreover, BPAF induced adipogenesis in the absence of the synthetic glucocorticoid dexamethasone.
Further, although BPAF significantly increased Tph1 mRNA levels, blocking its activity with parachlorophenylalanine (pCPA), did not block the adipogenic effects of BPAF. However, cotreatment with the MAO inhibitor, phenelzine, significantly decreased lipid accumulation and peroxisome proliferator activated receptor gamma (Pparg) expression. Therefore, these data demonstrate that BPAF may act as an obesogen and suggests that its action might be mediated, in part, by altered 5-HT signaling
McMaster University MASTER OF SCIENCE (2017) Hamilton, Ontario (Medical Sciences) TITLE: BPAF-Induced Adipogenesis in 3T3-L1 Cells: Role of Peripheral Serotonin Signaling AUTHOR: Kristina D. Wiggers, B.MSc. (University of Western Ontario) SUPERVISOR: Dr. Alison Holloway SUPERVISORY COMMITTEE: Dr. Warren Foster Dr. Gregory Steinberg
More information: Natasha Chernis et al. Bisphenol AF promotes inflammation in human white adipocytes, American Journal of Physiology-Cell Physiology (2019). DOI: 10.1152/ajpcell.00175.2019
Provided by American Physiological Society