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Abstract P121: Metabolic Influences Of Bisphenol F Exposure In Population-based Heterogeneous Stock Rats
Abstract   Peer reviewed

Abstract P121: Metabolic Influences Of Bisphenol F Exposure In Population-based Heterogeneous Stock Rats

Karen C Clark, Katie Holl, Derek Simonsen, Miriam Velez-Bermudez, Kai Wang, Leah Solberg Woods, Hans-Joachim Lehmler and Anne Kwtiek
Hypertension (Dallas, Tex. 1979), Vol.76(Suppl_1)
09/2020
DOI: 10.1161/hyp.76.suppl_1.P121

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Abstract

Bisphenol F (BPF) is marketed as a ‘safe’ substitute for bisphenol A (BPA), an endocrine disruptor associated with obesity and heart disease (i.e. cardiometabolic disease), in manufacturing polycarbonates and common consumer products. BPF’s environmental presence is growing and is detected in 66.5% of U.S. adults. Evidence of individual variation in bisphenol levels suggests that gene x environment (GxE) interactions influence cardiometabolic disease risk from bisphenol exposure. Few studies of BPF exposure in either humans or animals have been performed, thus health risks associated with BPF exposure are unknown. Traditional in vivo toxicity studies are performed in isogenic or genetically undefined outbred rodents, leading to conflicting results possibly due to GxE interactions. The N/NIH Heterogeneous Stock (HS) rats are a genetically heterogeneous population amenable to genetic study. Our overall study hypothesis is that BPF-induced cardiometabolic disease has underlying genetic risk, which can be identified using the HS rat model. The goal of this pilot project was to determine if BPF exposure affects growth and adiposity in HS rats. Weanling littermate pairs of male HS rats were randomly exposed to either vehicle (0.1% EtOH) or 1.125 mg BPF/L in 0.1% EtOH for five weeks in drinking water. Cardiometabolic measures, tissues, urine, and feces were taken. Our studies determined BPF exposure in HS rats significantly increases body growth (154.2 ± 3.0 g vs 160.9 ± 3.2 g, p=0.03). BPF exposure alters body composition seen in nuclear magnetic resonance measurements by increasing %fat (7.8 ± 0.3 % vs 8.4 ± 0.3 %; p=0.06), mirroring the significant increase in gonadal white adipose tissue (GWAT) mass (7.58 ± 0.29 mg/g vs 8.37 ± 0.34 mg/g, p=0.01) and perirenal white adipose tissue mass (10.6 ± 0.5 mg/g vs 12.2 ± 0.5 mg/g, p<0.01) in BPF-exposed males. Linear regressions of liver Ugt1a9 expression, an enzyme implicated in BPF metabolism, and %fat or GWAT mass were significantly different between exposure groups (%fat p=0.02, GWAT p=0.02), suggesting that Ugt1a9 expression is related to adiposity phenotype development in BPF-exposed rats. Our data suggest that BPF exposure increases body growth and adiposity, which are risk factors for cardiometabolic disease.

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