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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 tissue and 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. 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.
The hypothalamus, a part of the brain, is the main regulatory organ for human appetite. The neurones 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 (thyroxine regulates the metabolic rate), the hypothalamic-pituitary-adrenal axis and a large amount of other mechanisms.
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), 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 system and the cerebral cortex, project on the hypothalamus and modify appetite. This explains why in clinical depression and 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) 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.
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 (Prader-Willi syndrome).
Mechanisms controlling appetite are a potential target for weight loss drugs. Early anorectics were fenfluramine and phentermine. A more recent addition is sibutramine (Reductil®, Meridia®), 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.
- Appetite depressing drugs
- Dietary restraint
- Eating attitudes
- Eating disorders
References & Bibliography
- 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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