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).

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GIP receptor agonism blocks chemotherapy-induced nausea and vomiting

In collaboration with Eli Lilly, this work demonstrates in three different mammalian species that GIPR signaling is capable of antagonizing emesis and nausea induced by chemotherapy treatment by counteracting the shift toward an excitatory glutamatergic signaling in areas of the brain critical for the mediation of emesis and nausea. These results highlight a potential new clinical use for GIP analogs to increase the efficacy of current therapeutic regimes for the treatment of nausea and emesis in oncology patients.

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Tirzepatide suppresses palatable food intake by selectively reducing preference for fat in rodents

In collaboration with Eli Lilly, we showed that the dual GLP-1/GIP agonist Tirzepatide robustly decreases preference for palatable foods by selectively decreasing lipid consumption. Our preclinical findings highlight that promoting healthier food options may contribute to the weight-loss success of therapeutic Tirzepatide use for patients.

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Corrination of a GLP-1 Receptor Agonist for Glycemic Control without Emesis

In collaboration with Syracuse University professor Dr. Robert Doyle, our labs created a conjugated GLP-1R agonist (Cbi-Ex4) with reduced brain penetrance that enhances glycemic control without inducing emesis or anorexia. Our preclinical findings highlight its potential therapeutic use for patients seeking improved glycemic control without the loss of appetite and emesis characteristic of current GLP-1 therapeutics.

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GIP Receptor Agonism Attenuates GLP-1 Receptor Agonist Induced Nausea and Emesis in Preclinical Models

Our research uncovered that glucose-dependent insulinotropic polypeptide receptor (GIPR) signaling blocks emesis and attenuates illness behaviors elicited by GLP-1R activation, while maintaining reduced food intake, body weight loss, and improved glucose tolerance.