Troy Hornberger

The focus of my lab’s research is aimed at defining how mechanical signals are converted into the biochemical events that regulate skeletal muscle mass. For example, work from my lab has shown that signaling through the mammalian target of rapamycin (mTOR) is both necessary and sufficient for the induction of hypertrophy that occurs in response to mechanical loading. We have also demonstrated that mechanical stimuli activate mTOR signaling through a unique phosphoinositide 3-kinase (PI3K)-independent mechanism, and that this mechanism is distinct from the core pathways that are employed by growth factors and nutrients. As part of this work, we have collaborated with Joshua Coon to study proteomic and phosphoproteomic changes in skeletal muscle after contractile-stimulation as well as muscle immobilization. Currently, the work in my lab is focused on defining the components of this unique mechanism. To accomplish this goal, we employ a variety of model systems that are relevant to diabetes-related research. For instance, physical exercise is a well- recognized and effective treatment for Type II diabetes, and we are currently utilizing the resources in the mouse phenotyping and lipidomics cores to characterize what, in our opinion, will be the first physiologically relevant mouse model of human resistance exercise. I expect that this model in conjunction with my lab’s expertise in exercise physiology will make an important contribution to diabetes research on the UW campus.