Position title: Professor of Medicine and Vice Chair for Research
Dyslipidemia is a prominent feature of type 2 diabetes mellitus (T2DM) and is often reflected by higher levels of atherogenic low density lipoproteins (LDL) and lower levels of cardio-protective high density lipoproteins (HDL). Both LDL- and HDL-cholesterol levels influence beta-cell function, suggesting that dyslipidemia contributes to beta-cell failure and thus, the manifestation and progression of T2DM. Under conditions of oxidative stress, HDL becomes oxidatively-modified by reactive aldehydes and its function compromised. Interestingly, these same reactive aldehydes (acrolein or malondialdehyde) are also found in patients with diabetes and/or known to destroy islet cell function. We are testing the hypothesis that modified forms of HDL (i.e. modified by reactive aldehydes) promote the development of diabetes by impairing pancreatic beta-cell function. In other funded studies, we are using adipocytes differentiated from ear mesenchymal stem cells to investigate the role that SR-BI, the most physiologically relevant HDL receptor, plays in adipocyte metabolic processes, specifically as it relates to glucose and lipid metabolism.