The conversation between sensory neurons and adipose tissue about energy metabolism

Adipose tissue (fat) is commonly thought to be nothing more than a place to store energy. However, adipose tissue is very much alive—in fact, adipose tissue secretes factors (adipokines) that influence other tissues. Moreover, sensory neurons in the adipose tissue sense fat stores and relay this information to the brain. The brain then signals to other tissues (or the same tissue), to regulate energy metabolism depending on how much fat stores are available. Additionally, sensory neurons also communicate back to adipocytes, however, this direction of communication is less understood. My project focuses on exploring the role of sensory neuron to adipocyte communication, how this communication is affected during metabolic stress (obesity, exercise, etc.), and how this relates to systemic energy metabolism. We think that various metabolites that are increased in obesity and diabetes may dysregulate the communication between sensory neurons and adipose tissue leading to accelerated metabolic dysfunction. On the contrary, we think that metabolites that are increased during exercise may improve this communication, leading to improved systemic energy metabolism. This work could provide new and alternative approaches to improve insulin resistance, adipose dysfunction, and diabetes, and consequently open the field to a wide range of drugs and interventions.