The appetite is the desire to eat
food, felt as hunger. Appetite exists in all higher lifeforms, and serves to regulate adequate energy intake to maintain metabolic needs. It is regulated by a close interplay between the digestive tract, adipose tissueand the brain. Decreased desire to eat is termed anorexia, while polyphagia(or "hyperphagia") is increased eating. Disregulation of appetite contributes to anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder.
The regulation of appetite has been the subject of much research in the 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 hormones, and both the central and autonomic nervous systems.
hypothalamus, a part of the brain, is the main regulatory organ for human appetite. The neurons that regulate appetite appear to be mainly 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 vagal tone (the activity of the parasympathetic autonomic nervous system), stimulation of the thyroid( thyroxineregulates the metabolic rate), the hypothalamic-pituitary-adrenal axisand a large number of other mechanisms.
The hypothalamus senses external stimuli mainly through a number of hormones such as
leptin, ghrelin, PYY 3-36, orexinand 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), interleukins 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 systemand the cerebral cortex, project on the hypothalamus and modify appetite. This explains why in clinical depressionand 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
malnutritionon the one side or obesityand 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) 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. depression) and others.
Dysregulation of appetite lies at the root of
anorexia nervosa, bulimia nervosaand binge eating disorder. In addition, decreased response to satietymay promote development of obesity.
Various hereditary forms of obesity have been traced to defects in hypothalamic signalling (such as the leptin receptor and the MC-4 receptor), or are still awaiting characterisation (
Mechanisms controlling appetite are a potential target for weight loss drugs. Early
anorectics were fenfluramineand phentermine. A more recent addition is sibutraminewhich increases serotoninand noradrenalinelevels in the central nervous system. In addition, recent reports on recombinant PYY 3-36suggest that this agent may contribute to weight lossby suppressing appetite.
Given the epidemic proportions of
obesityin the Western world, developments in this area are expected to snowball in the near future, as dieting alone is ineffective in most obese adults.
* 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.
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