Frederick C. de Beer, MD

Our group investigates the impact of inflammation and insulin resistance on lipoprotein and cellular metabolism. In one project, we are investigating how inflammation and insulin resistance alters the metabolism and function of high-density lipoprotein (HDL). For decades, HDL has been considered to be the “good cholesterol” because individuals with high levels of HDL in their blood are at lower risk for cardiovascular disease (heart attack and stroke) compared to individuals with low HDL. HDL is thought to protect against cardiovascular disease through its ability to transport “bad” cholesterol that has accumulated in blood vessels back to the liver, where it can be removed from the body. Our group investigates the hypothesis that inflammation and insulin resistance interferes with HDL’s ability to carry out this protective function. Many of our studies focus on serum amyloid A (SAA). SAA is an acute phase reactant whose secretion by the liver can increase up to 1000-fold during severe inflammation, such as sepsis. Virtually all of the SAA in the blood is associated with HDL. We are investigating whether persistent elevations of SAA in individuals with chronic inflammation or insulin resistance leads to detrimental effects in blood vessels and other tissues. We also study secretory phospholipase A2 (sPLA2’s), a class of secreted enzymes that can hydrolyze phospholipids on cell membranes and lipoprotein particles. We have determined that their activity is increased during inflammation and are currently studying how these enzymes impact cell metabolism.