Appetite

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Appetite is the desire to eat food, felt as hunger. Appetite exists in all higher life-forms, 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. Dysregulation of appetite contributes to anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder.

Contents

[edit] Regulation

The regulation of appetite (the appestat) has been the subject of much research in the last decade[update]. 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.

[edit] Effector

The hypothalamus, a part of the brain, is the main regulatory organ for the 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 (thyroxine regulates the metabolic rate), the hypothalamic-pituitary-adrenal axis and a large number of other mechanisms. Opioid receptor-related processes in the nucleus accumbens and ventral pallidum effect the palatability of foods.[1]

[edit] 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), 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.

[edit] Role in disease

A limited or excessive appetite is not necessarily pathological. Abnormal appetite could be defined as eating habits causing malnutrition and related conditions such as obesity and its related problems.

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. Dyspepsia, also known as indigestion, can also affect appetite as one of its symptoms is feeling “overly full” soon after beginning a meal.[2]

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 MC-4 receptor), or are still awaiting characterisation (Prader-Willi syndrome).

[edit] Pharmacology

Mechanisms controlling appetite are a potential target for weight loss drugs. Early anorectics were fenfluramine and phentermine. A more recent addition is sibutramine which increases serotonin and noradrenaline levels in the central nervous system, but had to be withdrawn from the market when it was shown to have an adverse cardiovascular risk profile. Similarly, the appetite suppressant rimonabant (a cannabinoid receptor antagonist) had to be withdrawn when it was linked with worsening depression and increased risk of suicide. 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, and the fact that it is even increasing rapidly in some poorer countries, observers[who?] expect developments in this area to snowball in the near future. Dieting alone is ineffective in most obese adults – and even obese adults who successfully lose weight through dieting, often put weight back on afterwards.

[edit] References

  1. ^ Wassum KM, Ostlund SB, Maidment NT, Balleine BW. (2009). Distinct opioid circuits determine the palatability and the desirability of rewarding events. Proc Natl Acad Sci U S A. 106:12512–12517 PMID 19597155 doi:10.1073/pnas.0905874106
  2. ^ National Digestive Diseases Information Clearinghouse (NDDIC). Indigestion.
  • 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.
  • Olsen, AnneMarie. (2011). Manipulating fat content of familiar foods at test-meals does not affect intake and liking of these foods among children. 57(3), http://www.sciencedirect.com/science/article/pii/S019566631100523X

Bates, John E., Brechwald, Whitney A., Hill G., Laura, Kenneth, Dodge A., Orrell-Valente,Joan K.,Pettit, Gregory S. (2007). “Just three more bites”: An observational analysis of parents’ socialization of children’s eating at mealtime. Appetite, 42, 37-45.

[edit] See also

source: http://en.wikipedia.org/wiki/Appetite

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