Metabolic disease and stress-related disorders have long been known to exhibit significant comorbidity. Given the clinical relevance of both obesity and stress-related disorders, recent efforts in the lab have focused on understanding the mechanisms and identifying specific neural substrates that mediate the interaction between energy balance and stress response. The overlap in neural circuitry governing energy balance and stress-related physiological and behavioral responses plays a significant role in mediating the high degree of comorbidity between obesity and stress. Efforts to understand the relationship between energy balance and stress have primarily centered on the activation of common downstream neuroendocrine circuitry (e.g. hypothalamic pituitary adrenal [HPA] axis) however, much less is known about the common upstream neurobiological substrates. The GLP-1 system and its interaction with the central serotonergic system are of particular interest and are currently being explored by the lab.