Our laboratory is broadly interested in what drives feeding behavior. What makes us motivated to eat, and what signals tell us to stop eating? We use a variety of behavioral, physiological, and molecular techniques to address these questions at multiple levels and to understand how feeding-relevant neurohormonal signals act in the brain to stimulate or suppress food intake. We are particularly interested in studying physiological systems that are thought to be translationally relevant, in hopes that our research may inform better treatments for obesity and eventually a cure for this common disease.
A few of the lab’s current interests are described here. Please also see our Publications page for other work from our team!
Amylin signaling in the mesolimbic reward system
Amylin is a peptide hormone that reduces energy intake and body weight. We have shown previously that amylin receptor activation in the mesolimbic reward system of the brain is both physiologically and pharmacologically relevant for energy balance control. However, there are many questions that still remain as to how these effects occur. Currently, we are investigating how mesolimbic amylin signaling suppresses intake of dietary macronutrients. We also recognize that there is a major gap in the amylin literature in that few papers have investigated how amylin-mediated signaling suppresses feeding and weight gain in females. Therefore, another aim of our current work is to understand how mesolimbic amylin signaling interacts with estrogens to control feeding and food reward.
Neurobiology of feeding behavior in Prader-Willi Syndrome
Prader-Willi Syndrome (PWS) is a genetic disorder that results in overeating and weight gain. The neurobiological changes underlying the altered energy balance control in PWS remain unclear. MAGEL2, a gene known to be disrupted in PWS, is thought to play a role in the energy balance phenotype of this disorder. We are using a MAGEL2-deficient rat model to study how this gene contributes to energy intake, meal patterns, weight gain, and motivation for palatable foods. We are also investigating how the hindbrain responds to satiation signals in the context of MAGEL2 deficiency, as the hindbrain is a critical hub that integrates feeding-relevant information from the brain and periphery.
Microplastics and ingestive behavior
Microplastics are increasingly prevalent in the environment and are thought to be potentially obesogenic, but our understanding of their effects on feeding and drinking behavior is unclear. As part of a collaborative project with multiple labs at UB, we are investigating how exposure to microplastics may alter energy intake, drinking behaviors, and the gut microbiome.