Obesity is one of the principal risk factors for metabolic dysregulations, including Type 2 diabetes, as well as cardiovascular disease and stroke. As a consequence, obesity creates incredible emotional, health and economic burdens worldwide. We are in desperate need of new therapies to reduce the effects of obesity.
The long-term goal of my laboratory is to identify new therapeutic approaches to treat or prevent obesity-derived pathologies by understanding the physiologic and pathologic fundamental mechanisms that control adipose tissue development, growth and metabolism.
In my lab, we use innovative lineage tracing techniques that allow single-cell resolution and a combination of whole-genome expression profiling, metabolomics, biochemical, physiological and cell biology approaches to find new therapeutic interventions against obesity.
Our findings indicate that adipose tissue, in contrast to other tissues and organs, carries a complexity of multiple stem cell and fully differentiated cell populations with complex dynamics and plasticity capabilities. Exploiting this developmental heterogeneity in the formation of adipose tissues, we demonstrated that genetically modifying the activity of the critical insulin/Akt/mTOR signaling pathway between adipocyte lineages during development significantly affects fat distribution, which, interestingly, is reminiscent of fat distribution observed in humans.
My research was featured on the cover of Cell Metabolism and Trends in Cell Biology, and several of my publications were selected for “best of” or “highlights” sections of their respective journals. In 2018, I was awarded with the Career Development Award by the American Heart Association and in 2020, with the Trustee Award from Cincinnati Children’s Hospital Research Foundation.
Adipocytes; brown and white fat; animal models; adipocyte development and heterogeneity; insulin signaling; animal models
Assistant Professor, UC Department of Pediatrics
Endocrinology, Developmental Biology