
pmid: 18353447
Most of the drugs that have entered the market for treating obesity were originally developed to treat psychiatric diseases. During the past decade, understanding of the neural circuits that underlie food intake has increased considerably. Different aspects of ingestive behavior such as meal termination, meal initiation and overconsumption of highly rewarding and palatable foods are modulated by different neuroanatomical structures. Integration of the action of many signaling molecules (e.g. hormones, neurotransmitters and neuropeptides) in these structures results in a response that, ultimately, modulates food intake. Thus, the type of drug required by an obese patient might depend on the individual cause of obesity. In this article, we summarize the neural circuits that regulate food intake and we provide a framework for understanding how obesity drugs function. Several potential drug targets are expressed in different neural circuits, implying that current and future obesity drugs act on partially overlapping systems that control food intake.
Serotonin, Pro-Opiomelanocortin, Arcuate Nucleus of Hypothalamus, Brain, Satiation, Nucleus Accumbens, Norepinephrine, Animals, Humans, Peptide YY, Anti-Obesity Agents, Obesity
Serotonin, Pro-Opiomelanocortin, Arcuate Nucleus of Hypothalamus, Brain, Satiation, Nucleus Accumbens, Norepinephrine, Animals, Humans, Peptide YY, Anti-Obesity Agents, Obesity
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