Abstract
<dm:abstracts xmlns:dm="http://www.elsevier.com/xml/dm/dtd"><ce:abstract xmlns:ce="http://www.elsevier.com/xml/common/dtd" view="all" class="author" id="aep-abstract-id1"><ce:section-title>Publisher Summary</ce:section-title><ce:abstract-sec view="all" id="aep-abstract-sec-id1"><ce:simple-para id="fsabs003" view="all">Mechanisms that promote dietary intake are called orexigenic. Regulation of intake behavior is closely integrated with other brain functions and the control of energy metabolism. Hormones, such as insulin, that were originally associated with the regulation of glucose utilization and other metabolic functions are now believed to directly impact appetite. Much of the activity related to appetite perception and intake regulation has been located to the arcuate nucleus of the hypothalamus near the third ventricle, the nearby ventromedial nucleus, and lateral areas of the hypothalamus. Increased expression of the oncogene c-fos in some of these brain regions correlates with appetite perception. NPY/melanocortin neurons, which are located mainly in the arcuate nucleus, constitute a significant portion of the appetite perception circuitry. One type of this neuron is characterized by its production of neuropeptide Y (NPY) and agouti-related protein (AgRP). Production of melanocortin characterizes the second type of neurons. The action of NPY/AgRP neurons on other neurons nearby stimulates the perception of appetite. The binding of melanocortin to melanocortin receptor 4 (Mc4r) on hypothalamic neurons inhibits appetite. AgRP specifically blocks the binding of melanocortin to Mc4r and other melanocortin receptors (Mc I rand Mc3r). Several types of neurons that are intimately involved in the regulation of appetite use serotonin as a neurotransmitter. Food intake stimulates the release of serotonin by such neurons and thereby induces a feeling of satiation. Various drugs that increase the availability of serotonin induce weight loss, and serious side-effects like pulmonary hypertension and heart valve damage.</ce:simple-para></ce:abstract-sec></ce:abstract></dm:abstracts>
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