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Laboratory of Regulatory Systems Neuroscience
University of Pennsylvania
The dramatic increase in the prevalence of obese and overweight individuals has intensified interest in obesity as a disease with significant health consequences and co-morbidities (e.g., type 2 diabetes, cardiovascular disease, cancer). Feeding-related pathologies are not limited to those associated with excess food consumption, but also include those related to insufficient food consumption such as failure to thrive, food selectivity, early satiety and dyspepsia. It is remarkable that despite the increased prevalence of these pathologies of feeding in humans of all ages, there are no effective pharmacological treatments currently available. The development of new and effective pharmacotherapies relies on findings from basic research on the neurobiology of energy balance. Our lab is focused on expanding knowledge of the neural circuits, neurochemical systems, and signaling pathways that contribute to the control of food intake and energy expenditure. Unique to our approach is the perspective that the neural control of energy balance is anatomically distributed rather than centered in any one region of the brain. This perspective leads us to examine the neural processing of peripherally generated neural signals (e.g., vagal afferent response to ingested food) and blood-born correlates of energy status signals (e.g., leptin, ghrelin) that act at multiple brain nuclei including but not limited to the caudal brainstem (e.g. nucleus tractus solitarius, parabrachial nucleus, caudal raphe), midbrain (e.g. ventral tegmental area), hypothalamus, hippocampus, and nucleus accumbens. Also influencing our work is the idea that the environmental factors that drive feeding behavior such as context, and learning as well as food palatability and its impact on reward are extremely important in understanding the control of feeding behavior, and like satiation and energy status signals, are also not controlled by distinct and unique neural circuits. Rather, our perspective is that each of these factors may involve signaling in anatomically distributed nuclei, and each nucleus may be involved in several functional controls of feeding.
NTS leptin receptor signaling is critical to food intake control.
Glucagon-like peptide-1 receptor signaling and energy balance: contributions from hindbrain and other nuclei.
Ventral hippocampal energy status signaling contributes to food intake control.
Hindbrain signal processing contributes to food motivation and reward.
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