poxia and Adipocyte Lipid Metabolism 7 Hypoxia and Adipocyte Lipid Metabolism populations and increase assay signal. Finally and importantly, the effect of 1820332 hypoxia on HBS was modest, mediating only a 0.8-fold decrease in HBS. Nonetheless, this effect was reproducible, statistically significant, and identical 
with two different assays. Furthermore, the effects of azaserine and glucosamine on adipocyte lipid metabolism, while statistically significant, were of similarly low magnitudes. These low magnitude effects suggest that HBS is likely one of many factors that mediates hypoxia’s effects on adipocyte lipid metabolism. Off-target effects of azaserine and glucosamine may further contribute to these modest effects. Future research will determine the importance of HBS in mediating hypoxia’s effects on adipocyte metabolism. Limitations in human subjects, tissue availability, and cell yield precluded analysis of all aspects of lipid metabolism including the effects of known mediators of lipolysis and FAO in the AEB 071 site context of hypoxia, such as insulin, adiponectin, and other stimuli, as well as rigorous correlation of in vitro results with clinical characteristics such as the presence of metabolic disease. Future research will be dedicated to studying these details of lipid metabolism. Conclusions We demonstrate that hypoxia shifts adipocyte lipid metabolism towards a pro-lipolytic, anti-lipogenic phenotype, an effect that would be expected to impair lipid buffering capacity and predispose to systemic lipotoxicity. Furthermore, we demonstrate that down-regulation of HBS is a potential underlying mechanism of hypoxia-mediated alterations in human adipocyte lipid metabolism. These observations identify HBS-related mediators and other hypoxia-inducible molecules as targets to regulate adipocyte metabolism. 12176911 Acknowledgments We wish to acknowledge Aurelie Snyder and the Advanced Light Microscopy Core at The Jungers Center at OHSU for technical assistance with immunofluoresence microscopy.