The prevalence of obesity has exploded over the past 40 years. The biological systems that underlie the excessive feeding behavior contributing to obesity onset remain poorly understood. Our research goal is to discover the neural systems and psychological processes that control feeding behavior, with a particular focus on understanding the neurobiological substrates that regulate obesity-promoting behaviors such as food impulsivity and environmental cue-induced feeding.
Food intake and body weight regulation are heavily influenced by endocrine and neuropeptidergic signals produced in the peripheral organs and/or in the brain (e.g., ghrelin, glucagon-like peptide-1, melanin-concentrating hormone, orexin, amylin) that act on receptors expressed in the brain's cognitive and reward circuitry. At the center of our research focus is the hippocampus, a brain region traditionally linked with the control of learning and memory. Our research has shown that the hippocampus regulates higher-order aspects of feeding behavior, in part, by detecting and utilizing circulating hormonal and neuropeptidergic signals. We utilize behavioral, neuropharmacological, neuroanatomical, chemogenetic, genetic, and molecular research strategies to explore how endocrine and neuropeptide systems act in the hippocampus and interconnected brain areas to increase (or decrease) food-motivated behavior. Our goal is to provide insight into the biology and psychology underlying the excessive food intake that is driving up obesity rates.
Another primary focus of our lab is to study how the brain is negatively impacted by dietary and metabolic factors. Saturated fatty acid and refined carbohydrate (i.e., sugar) consumption not only contributes to obesity development, but also produces deficits in learning and memory capabilities and can even increase the risk for developing dementia. We are currently examining the specific causal dietary factors, critical developmental periods, and neurobiological mechanisms underlying diet-induced hippocampal dysfunction and cognitive decline.