Neuroendocrine Control of Energy Balance
Our laboratory’s overarching goal seeks to understand the neuroendocrine systems regulating energy balance and motivated behaviors. Using multiple approaches from the cell to the whole organism and extensively examine the role of various neuroendocrine signaling systems (e.g., GLP-1, leptin, amylin, CCK, serotonin, glutamate, and dopamine) in peripheral and central control of food intake and body weight regulation.
Overall, our research program takes a novel systems-neuroscience approach aimed at enhancing the development of realistic pharmacological-based therapeutics to treat obesity and associated comorbidities (e.g. obesity, eating disorders, diabetes, drug addiction and nausea / malaise).
The locus coeruleus contributes to the anorectic, nausea, and autonomic physiological effects of glucagon-like peptide-1
These data contribute to a growing body of evidence that highlights the LC as a feeding-relevant nucleus. As the LC is known to express receptors for other neuropeptides relevant to energy balance regulation, future investigations aimed at characterizing the endogenous mechanism by which the LC participates in food intake control are warranted. Here, we characterize a previously unexplored site of action for endogenous and exogenous GLP-1 signaling. We show that LC GLP-1R activation suppresses food intake, engages autonomic responses, and results in illness-like behaviors. This insight is necessary to advance clinical strategies for the treatment of obesity with improved GLP-1 analogs, with the hope of mitigating the nausea pervasive to current existing GLP-1–based pharmacotherapies.
GLP-1 Receptors action on brainstem GABA neurons
Examining the contribution of nucleus tractus solitarius (NTS) glucagon-like peptide-1 receptors (GLP-1Rs) to the anorectic potential of the FDA-approved obesity drug liraglutide and highlights a phenotypically distinct (GABAergic) population of neurons within the NTS that express the GLP-1R and are involved in the mediation of liraglutide signaling