My long-term objective is to develop a career in the field of cardiovascular research with a special interest in understanding the mechanisms by which diet-induced obesity contributes to the development of cardiovascular disease. I aspire to become an independent investigator in a research-intensive environment such as the University of Utah. My long-term scientific goal is to discover strategies that can reduce diet-induced obesity and thus, limit a major risk factor for cardiovascular disease. This goal has specific objectives that include: (a) investigate the mechanisms involved in ROS production in WAT in DIO; (b) characterizing the mechanisms by which ROS contribute to fat expansion in DIO and (c) developing strategies that can limit ROS production thereby preventing diet-induced fat expansion. The specific aims of this application: (1) Will investigate the cell type and the mechanisms involved in ROS production in WAT of mice fed a HFD. This goal will determine if ROS are being generated in specific cells within WAT and if mitochondrial alterations in these cells are responsible for increased ROS (2) Will determine if increased mitochondrial superoxide production modulates the proliferative capacity of WAT progenitor cells in mice fed-HFD. This aim will examine if increased superoxide production in WAT progenitor cells accelerate their proliferation 3) Will determine and characterize the redox-sensitive signaling pathways involved in WAT progenitor cell proliferation in DIO. This goal will investigate first the molecular pathways involved in HFD-induced WAT progenitor cells proliferation and second if these pathways are redox-sensitive. This research is highly significant to the field because obesity is a risk factor for cardiovascular disease and is dramatically increasing particularly among children as a result of increased caloric intake and limited physical activity. The study proposed may identify novel targets for the treatment and the prevention of DIO.
|Program type||Scientist Development Grant|
|Effective start/end date||07/01/2009 → 06/30/2013|