My research interests are focused on the role of Apolipoprotein E (ApoE) in the development of cardiovascular disease.  Specifically, I am interested in the regulatory effects of ApoE on lipid metabolism in a diabetic background.  Apolipoprotein E (ApoE) is associated with circulating lipoproteins, specifically very low density lipoproteins (VLDL) and high density lipoproteins (HDL).  The pathways of lipid and glucose metabolism are intricately linked by the action of many regulatory molecules.  This link is notably evidenced by the dyslipidemia commonly seen in diabetic patients, which increases their risk and rate of development of atherosclerosis, as well as in the metabolic syndrome.  As it has been shown to mediate lipid metabolism in normo-lipidemic patients, ApoE likely also plays a role in the changes in lipid profile seen in diabetics.  
 Our lab has previously created mouse models which express the different human ApoE isoforms and mimic the lipid profiles typically seen in humans.  The interactions between lipid profiles, ApoE isoforms, and atherosclerosis that can be demonstrated in humanized mouse models make a strong case for using these models to look for interactions between these same variables and the development of diabetic vascular complications.  We are employing several methods of generating diabetes in these models, including targeted destruction of insulin producing b-cells in the pancreas, and inter-crossing with models of severe insulin resistance and Insulin-Dependent Diabetes Mellitus.