Gary J. Schwartz, Ph.D., studies how the gut and the brain interact with each other to regulate food intake and associated metabolic processes.  Dr. Schwartz and his colleagues aim to identify therapeutic targets for eating behaviors associated with obesity, diabetes and related diseases.

Our research focuses on the sensory neural controls of energy homeostasis in health and disease. We use rodent models to examine how food stimuli act at oral and gastrointestinal sites to affect food intake, energy balance, and gastrointestinal physiology.We approach this problem from multiple levels of analysis including behavioral, physiological, neurophysiological, and molecular-genetic. We have identified the type of food stimuli that activate vagal and splanchnic sensory fibers supplying the gut, and have revealed the extent to which these stimuli influence gut-brain communication. Our most recent efforts involve the analysis of gut-brain communication in the control of energy homeostasis in mouse models of obesity and diabetes.We have identified neurons in the periphery, brainstem and hypothalamus that integrate food-elicited signals with peptide signals that have profound effects food intake and metabolism. Data from these studies reveal that central hypothalamic and brainstem neuropeptides affect food intake and body weight by modulating the neural potency of food stimulated signals from the mouth and gut. This novel, synthetic conceptual framework is critical because it links forebrain hypothalamic structures, long known to be involved in the control of energy balance, to the sensory and motor systems in the brainstem that control ingestion, digestion, and metabolic processing of food. Future studies will use genetic mouse models of obesity and diabetes with targeted conditional neuropeptide/ receptor knockdown or replacement to determine how central neuropeptide signaling affects the neural processing of metabolic sensory signals critical to energy homeostasis.