Ghrelin, a 28-amino acid acylated peptide predominantly produced by the stomach, displays strong GH-releasing activity mediated by the hypothalamic-pituitary GH secretagogues (GHS) receptors (GHS-R) which had been shown specific for a family of synthetic, orally active molecules known as GHS. However, ghrelin and GHS, acting on central and peripheral receptors, also exert other actions. These include influence on pituitary functions, orexigenic action, influence on exocrine and endocrine gastro-entero-pancreatic functions, cardiovascular and anti-proliferative effects. In particular, the effect of ghrelin in promoting food intake and modulating energy metabolism strongly suggested that ghrelin has a key role in managing the neuroendocrine and metabolic response to starvation and that could be involved in the pathogenesis and/or in the metabolic and neuro-hormonal alterations of obesity and eating disorders. Although specific alterations in ghrelin secretion and/or action in obesity and anorexia nervosa (AN) have already been reported, the possibility that ghrelin analogues acting as agonists or antagonists has clinical perspectives for treatment of eating disorders presently remains a dream.
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