Obesity, which is defined as an excessive increase in white adipose tissue (fat) mass, is the leading public health concern of modern society. Despite the importance of fat in human disease our understanding of the regulation of fat mass is extremely limited. The research in my laboratory is directed toward elucidating the cellular and molecular mechanisms that regulate fat mass and contribute to the development of obesity and obesity associated diseases, such as diabetes and heart disease.
Despite the dynamic nature of fat mass, fat cell number is tightly regulated. During normal development, a ‘setpoint’ of fat cell number is established. In obesity, both fat cell size and fat cell number increase, establishing a new, higher setpoint. As fat cells are post-mitotic, new fat cells are produced by the proliferation and differentiation of fat stem cells. However, the identity of these stem cells remained elusive until recently, when our lab identified early fat cell progenitors in mice. We have since characterized the cellular pathway of adipogenesis in vivo, opening the door for our current studies how fat cells form during normal development and how the food we eat can lead to obesity.
We take several approaches to accomplish our research goals, employing mouse models of human disease, human primary cell culture, genomic and proteomic techniques as well as novel mouse models for the study of fat regulation. Determining the intrinsic molecular mechanisms that regulate fat mass is imperative for understanding the development of obesity and obesity related pathologies, and will lead to the generation of novel therapeutics for the treatment of obesity and its associated pathologies.