In normal individuals fasting and weight loss increase hunger by multiple mechanisms (decreased serum levels of leptin, insulin, and blood glucose and increased levels of ghrelin). At the level of the hypothalamus there is an increase in the potent orexigenic neuropeptide Y and other changes in neurotransmitters secondary to the fasting state. Some of these neurotransmitter changes may be the cause or a mechanism of anorexia nervosa, and for this reason they have received considerable attention in the past several years. It is important to understand that appetite control is a very complex hypothalamic function that involves many local and systemic neuropeptides, amines, and hormones.
Abnormal serotonin activity has been found in the brain of women with anorexia nervosa. An area in the chromosome 1 (p36.3-34.3) that contains genes for the serotonin 1D receptor and for the opioid delta receptor was associated with patients with anorexia nervosa by linkage analysis. One polymorphism in the Agouti related protein (Ala67Thr) has also been found associated with anorexia nervosa. Melanocortin system stimulants in the hypothalamus, such as Agouti related protein, are also involved in appetite and energy regulation. On the other hand, these genetic abnormalities may amount to only a biological tendency and do not explain the relatively short term of the illness during a life time or the changes in prevalence in the past decades.
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