America’s healthcare system is facing a new epidemic: metabolic disease. With almost one-third of the population dealing with obesity, metabolic disease is on the rise. Nonalcoholic fatty liver disease (NAFLD) is one of these metabolic diseases. The definitive cause of NAFLD is unknown, and with more and more people affected each year, the need for treatment is growing. Fatty acids are an essential macromolecule needed for various cellular functions, however, in excess, they can be damaging to cells. The goal of this research is to identify the role that oleate and palmitate, unsaturated and saturated fatty acids respectively, play in cellular signaling in relation to NAFLD. Preliminary data from our laboratory has identified cytokine-induced neutrophil chemoattractant 1 (CINC-1) and vascular endothelial growth factor (VEGF) as cytokine signals believed to play a role in cellular death in relation to fatty acid excess. H411e rat hepatoma cells were treated with either oleate, palmitate, an ethanol control, or both fatty acids. ELISAs were performed to detect CINC1 and VEGF in all treatment groups. The treatment group with a significantly higher signal concentration for both CINC1 and VEGF was the palmitate group; the signal was three times higher for CINC1 than other treatment groups. Concentration data were normalized to total protein for all treatment groups. Future goals include research on the effect of fatty acid concentration and time course on CINC1 and VEGF signal concentration.<br/>

Fatty acid effects on CINC-1 and VEGF signaling in rat hepatoma cells

2019 Spring National Meeting

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