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Appetite

The appetite is the desireto eatfood, felt as hunger. Appetite exists in all higher lifeforms, and serves to regulate adequate energy intake to maintain metabolicneeds. 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. Dysregulation of appetite contributes to anorexia nervosaand cachexiaon one side, and obesityon the other side of the spectrum.

Inhaltsverzeichnis

1 Regulation
- 1.1 Effector
- 1.2 Sensor
2 Role in disease
3 Pharmacology
4 Further reading

Regulation

The regulation of appetite has been the subject of much research in the last decade. Breakthroughs included the discovery, in 1995, 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 centraland autonomic nervous systems.

Effector

The hypothalamus, a part of the brain, is the main regulatory organ for appetite. The neuronesthat 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 vagaltone (the activity of the parasympathicautonomic nervous system), stimulation of the thyroid(thyroxineregulates the metabolic rate), the hypothalamic-pituitary-adrenal axisand a large amount of other mechanisms.

Sensor

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 factoralpha (TNFα), interleukins1 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. Likely, 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 MSH-4receptor), or are still awaiting characterisation (Prader-Willi syndrome).

Pharmacology

Mechanisms controlling appetite are a potential target for weight loss drugs. Early anorecticswere fenfluramineand phentermine. A more recent addition is sibutramine(Reductil®, Meridia®), which increases serotoninand noradrenalinelevels in the central nervous system. In addition, recent reports on recombinantPYY 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.