Our research program is exploring the neurobiological controls of food intake and body weight regulation.
The prevalence of obesity has exploded over the past 30 years. The neurobiological systems that underlie the excessive feeding behavior contributing to obesity onset remain poorly understood. Our goal is to explore the neurobiological control of feeding behavior, including higher-order decisions about whether to eat or not to eat, what to consume, and how much of it to consume.
These decisions 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, 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 region traditionally linked with the control of learning and memory. We've recently shown that the hippocampus regulates higher-order aspects of feeding behavior by detecting and utilizing circulating hormonal signals. Our research approach uses neuropharmacological, neuroanatomical, chemogenetic, behavioral, and other research strategies to explore how endocrine and neuropeptidergic 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 in Western cultures.
A second and related 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 Alzheimer's pathology. We are currently examining the specific causal dietary factors, critical developmental periods, and neurobiological mechanisms underlying diet-induced hippocampal dysfunction and cognitive decline.
Our research is funded by NIH: DK104897, DK105155, DK118402, the USC Diabetes and Obesity Research Institute, The Obesity Society, and the following NIH fellowships: DK111158, DK118944, DK104897S1.