Metabolic Influences of Bisphenol F Exposure in Population-based Heterogeneous Stock rats
Poster sessions are particularly prominent at academic conferences. Posters are usually one frame of a powerpoint (or similar) presentation and are represented at full resolution to make them zoomable.
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 in common consumer products (e.g. food packaging). BPF’s environmental presence is growing rapidly and is detected in 66.5% of U.S. adults. There is evidence of individual variation in bisphenol levels, suggesting that genetic variation or gene x environment (GxE) interactions influence risk of cardiometabolic disease due to bisphenol exposure. Characterizing the cardiometabolic effects of BPF in either humans or animal models has not been performed, and the health risks associated with BPF exposure are vastly unknown. Traditional in vivo toxicity studies are performed in genetically undefined, outbred rats or genetically homogeneous, inbred mice, leading to conflicting results possibly due to GxE interactions. The N/NIH Heterogeneous Stock (HS) rats are a genetically heterogeneous rat population that is amenable to genetic study. Our overall hypothesis is that BPF exposure is a cardiometabolic disease risk factor based on underlying genetic susceptibility, which can be identified using the HS rat model.
We previously demonstrated that five weeks of post-wean BPF exposure significantly impacts body growth and adiposity in male HS rats. The goal of this project was to determine if maternal BPF exposure also influences growth and adiposity in HS rats, since maternal exposure to BPA is known to impact the metabolic health of both the mother and offspring