Lipoprotein Metabolism
Atherosclerosis
HDL Receptor SR-BI
Viral vector mediated gene transfer

Dr. Webb’s research focuses on secretary phospholipase A2’s (sPLA2), a group of enzymes that hydrolyze phospholipids at the sn-2 position to liberate free fatty acids and lysophospholipids. Funded projects in the Webb lab include studying the role of sPLA2’s in lipoprotein metabolism, atherosclerosis, and abdominal aortic aneurysm formation using mouse models. In recent studies, her laboratory made the novel finding that one member of the sPLA2 family, Group X sPLA2, plays a previously unrecognized role in adipose tissue. Mice deficient in Group X sPLA2 have significantly increased adiposity compared to wild-type mice, yet are protected from high fat diet-induced insulin resistance. Current studies in her lab are testing the hypothesis that Group X sPLA2 in adipose tissue modulates the equilibrium between adipocyte lipid storage and lipid catabolism and thereby regulates adipocyte hypertrophy, adipose tissue inflammation, free fatty acid flux, and whole body insulin sensitivity. Dr. Webb anticipates that her research will show that enhancing the capacity of adipose tissue to store fat will have a beneficial effect on inflammation and insulin sensitivity in the setting of caloric excess. These studies could provide new strategies to prevent or treat metabolic consequences of obesity.