from Section VI - Eating Disorders
Published online by Cambridge University Press: 10 January 2011
Introduction
The preceding two chapters synthesize the evidence from imaging studies which explore normal eating behavior, and the clinical manifestations of disturbed eating behavior ranging from obesity through to anorexia nervosa. Both chapters have been written by individuals with a high level of expertise and they contain a wealth of information. For those of us struggling to keep up and assimilate this knowledge base, it is easy to get lost in the detail. I have therefore introduced a simple diagram to help to navigate a path through this information. In this diagram the central control of appetite is simplified into three basic elements (Figure 35.1).
First, there is the homeostatic system (Nutrostat) centered mainly in the brain stem and hypothalamus that integrates metabolic markers (insulin, leptin, PYY, ghrelin, etc.), and information from the gastrointestinal tract, and has outputs such as hunger, fullness and autonomic nervous activity. The neurotransmitters involved include MCH, alpha MSH, agouti-related peptide, orexin and neuropeptide Y. Second, there is the drive and reward system (Hedonic) centered within the mesolimbic system and striatum, which registers the salience and reward value associated with food and is involved in signaling the drive to eat. This has inputs from sensory organs and the hippocampus. The key neurotransmitters in this system are dopamine and opioids. The third system, the self-regulatory system, includes frontostriatal circuits involving 5-HT, amongst other neurotransmitters. This exerts control over the other more reflexive, automatic components and serves to integrate appetite into a personal and societal framework.
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