Neurobiology of nutrition and obesity.
In the course of evolution, the need to eat has powerfully shaped biological structure and function. As a result, nutrient-depletion signals strongly activate neural mechanisms that orchestrate foraging, appetitive, and ingestive behaviors and at the same time instigate an internal energy savings mode through autonomic, endocrine, and peripheral cellular mechanisms. Although the hypothalamus and brainstem play crucial roles in the initiation and coordination of these responses, it is the integrated action of a much more complex and distributed neural system that is engaged in this fundamental survival reflex. In our modern, media-driven and mechanized environment of plenty, it is particularly important to recognize the neural systems responsible for learning and memory, reward, emotions and mood, decision-making and choice, and dealing with stress. These neural systems appear to powerfully assist the hypothalamic regulator in defending the lower limits of body weight, but they do little in overcoming its inherent weakness to defend over-nutrition and the upper limits of body weight and adiposity. The challenge is to define the role of these extrahypothalamic brain structures involved in the cognitive, rewarding, and emotional aspects of ingestive and physical activity behaviors and their relationship to the homeostatic regulator, and to assess the capacity of these mechanisms in predisposing to obesity.
Morrison
Christopher D
CD
Neurosignaling Laboratory, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, Louisiana 70808, USA.
Berthoud
Hans-Rudolf
HR
D001066:Appetite / Q000235:genetics / Q000502:physiology; D005075:Biological Evolution; D001921:Brain / Q000502:physiology*; D002149:Energy Intake / Q000235:genetics / Q000502:physiology; D004734:Energy Metabolism / Q000235:genetics / Q000502:physiology*; D006706:Homeostasis; D006801:Humans; D007031:Hypothalamus / Q000502:physiology*; D009434:Neural Pathways / Q000502:physiology; D009765:Obesity / Q000209:etiology / Q000235:genetics*