Appetite
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2008-07-06T20:02:58Z
SJP
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Reverted edits by [[Special:Contributions/76.28.40.209|76.28.40.209]] to last version by SJP (using [[WP:HG|Huggle]])
{{for|the mineral|Apatite}}
The '''appetite''' is the desire to [[eating|eat]] [[food]], felt as [[hunger]]. Appetite exists in all higher lifeforms, and serves to regulate adequate energy intake to maintain [[metabolism|metabolic]] needs. It is regulated by a close interplay between the [[digestive tract]], [[adipose tissue]] and the [[brain]]. Decreased desire to eat is termed [[anorexia (symptom)|anorexia]], while [[polyphagia]] (or "hyperphagia") is increased eating. Disregulation of appetite contributes to [[anorexia nervosa]], [[bulimia nervosa]], [[cachexia]], [[overeating]], and [[binge eating disorder]].
==Regulation==
The regulation of appetite has been the subject of much research in the [[as of 2004|last decade]]. Breakthroughs included the discovery, in [[1994]], of [[leptin]], a hormone that appeared to provide negative feedback. Later studies showed that appetite regulation is an immensely complex process involving the [[gastrointestinal tract]], many [[hormone]]s, and both the [[central nervous system|central]] and [[autonomic nervous system]]s.
===Effector===
The [[hypothalamus]], a part of the brain, is the main regulatory organ for human appetite. The [[neuron]]s that regulate appetite appear to be mainly [[serotonin|serotonergic]], although [[neuropeptide Y]] (NPY) and [[Agouti-related peptide]] (AGRP) also play a vital role. Hypothalamocortical and hypothalamolimbic projections contribute to the awareness of hunger, and the somatic processes controlled by the hypothalamus include [[vagus nerve|vagal]] tone (the activity of the [[Parasympathetic nervous system|parasympathetic]] [[autonomic nervous system]]), stimulation of the [[thyroid]] ([[thyroxine]] regulates the metabolic rate), the [[hypothalamic-pituitary-adrenal axis]] and a large number of other mechanisms.
===Sensor===
The hypothalamus senses external stimuli mainly through a number of hormones such as [[leptin]], [[ghrelin]], [[PYY 3-36]], [[orexin]] and [[cholecystokinin]]; all modify the hypothalamic response. They are produced by the digestive tract and by [[adipose tissue]] (leptin). Systemic mediators, such as [[tumor necrosis factor-alpha]] (TNFα), [[interleukin]]s 1 and 6 and [[corticotropin-releasing hormone]] (CRH) influence appetite negatively; this mechanism explains why ill people often eat less.
In addition, the [[biological clock]] (which is regulated by the hypothalamus) modifies hunger. Processes from other cerebral loci, such as from the [[limbic system]] and the [[cerebral cortex]], project on the hypothalamus and modify appetite. This explains why in [[clinical depression]] and [[stress (medicine)|stress]], energy intake can change quite drastically.
==Role in disease==
A limited or excessive appetite is not necessarily pathological. Abnormal appetite could be defined as eating habits causing [[malnutrition]] on the one side or [[obesity]] and its related problems on the other.
Both genetic and environmental factors may regulate appetite, and abnormalities in either may lead to abnormal appetite. Poor appetite ([[anorexia (symptom)|anorexia]]) may have numerous causes, but may be a result of physical (infectious, autoimmune or malignant disease) or psychological (stress, mental disorders) factors. Likewise, [[hyperphagia]] (excessive eating) may be a result of hormonal imbalances, mental disorders (e.g. [[clinical depression|depression]]) and others.
Dysregulation of appetite lies at the root of [[anorexia nervosa]], [[bulimia nervosa]] and [[binge eating disorder]]. In addition, decreased response to [[satiety]] may promote development of [[obesity]].
Various hereditary forms of obesity have been traced to defects in hypothalamic signalling (such as the leptin receptor and the [[melanocyte-stimulating hormone|MC-4]] receptor), or are still awaiting characterisation ([[Prader-Willi syndrome]]).
==Pharmacology==
Mechanisms controlling appetite are a potential target for weight loss drugs. Early [[anorectic]]s were [[fenfluramine]] and [[phentermine]]. A more recent addition is [[sibutramine]] which increases [[serotonin]] and [[noradrenaline]] levels in the [[central nervous system]]. In addition, recent reports on [[recombinant]] [[PYY 3-36]] suggest that this agent may contribute to [[weight loss]] by suppressing appetite.
Given the epidemic proportions of [[obesity]] in the Western world, developments in this area are expected to snowball in the near future, as dieting alone is ineffective in most obese adults.
==Further reading==
* Neary NM, Goldstone AP, Bloom SR. ''Appetite regulation: from the gut to the hypothalamus.'' Clin Endocrinol (Oxford) 2004;60:153-60. PMID 14725674.
* Wynne K, Stanley S, Bloom S. ''The gut and regulation of body weight.'' J Clin Endocrinol Metab 2004;89:2576–82. PMID 15181026.
[[Category:Endocrinology]]
[[Category:Food and drink]]
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